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CTL/CD8+ Epitope Variants and Escape Mutations

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List of Mutation types

Data last updated at 2014-02-07 10:41:32-07
Epitope ID Epitope Name Variant ID Subtype Epitope Subtype Variant Subtype Protein HXB2 start HXB2 end Subprotein HXB2 DNA Contig HLA Epitope Variant Epitope Mutation (epitope) Mutation (protein) Mutation Type Code Mutation Type Description Methods Note References
54532 AI14 1016 B B A, M-group Gag 5 19 p17(5-19) 802..846   ASVLSGGELDRWEKI ASVLSGGkLDaWEKI R11A, E8K R15A, E12K SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy No cross-recognition of this variant was seen across clades or intra-clade central sequences. Malhotra2007
54532 AI14 1017 B B C Gag 5 19 p17(5-19) 802..846   ASVLSGGELDRWEKI ASiLrGGkLDkWEKI R11K, V3I, S5R, E8K R15K, V7I, S9R, E12K SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy No cross-recognition of this variant was seen across clades or intra-clade central sequences. Malhotra2007
54532 AI14 1018 B B B Gag 5 19 p17(5-19) 802..846   ASVLSGGELDRWEKI ASVLSGGkLDkWEKI R11K, E8K R15K, E12K SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy No cross-recognition of this variant was seen across clades or intra-clade central sequences. Malhotra2007
54532 AI14 1019 B B B Gag 5 19 p17(5-19) 802..846   ASVLSGGELDRWEKI ASVLSGGELDkWEKI R11K R15K SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy No cross-recognition of this variant was seen across clades or intra-clade central sequences. Malhotra2007
53591 Gag 1.2 54   B CRF02_AG Gag 8 18 p17(8-18) 811..843   LSGGELDRWEK LSGGkLDaWEK E5K, R8A E12K, R15A SNSF subtype-specific non-susceptible form Intracellular cytokine staining, T-cell Elispot CRF02 form, LSGGkLDaWEK, does not cross-react with the B clade LSGGELDRWEK elicited response. Amara2005a
53844 GI9 1569 B     Gag 11 19 p17(11-19) 820..846 B40 GELDRWEKI GELDRWkKI E7K E17K DR, LE diminished response, literature escape CD8 T-cell Elispot - IFNy, Sequence This variant from the HXB2 sequence was present in the restricting HLA-B40-carrying mother, M-1002, but was never detected in her non-HLA-B40-carrying infant, P-1031. Decreased recognition of the E17K variant relative to the index epitope was seen in the mother. Sanchez-Merino2005
56027 GI9(p17) 1903 B B B Gag 11 19 p17(11-19) 820..846   GQLDRWEKI GeLDRWEKI Q2E Q12E OV observed variant CD8 T-cell Elispot - IFNy, Sequence This Asian B Clade optimal epitope differs from the consensus B at one position. It is predicted to be HLA-B40 restricted. Experimentally, B clade consensus peptide was used to challenge CTL response in subjects commonly carrying the Asian B-type epitope. Zhai2008
55632   11 A, CRF02_AG, CRF01_AE A, AG AE Gag 11 22 p17(11-22) 820..855   GKLDSWEKIRLR GKLDaWEKIRLR S5A S15A SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy 1 subject responded to peptide GKLDSWEKIRLR from subtypes CRF02_AG and A, and to peptide GKLDaWEKIRLR from subtype CRF01_AE. Aidoo2008
54629 GAG-03 1957 B B C Gag 17 34 p17(17-34) 838..891   EKIRLRPGGKKKYRLKHL EKIRLRPGGKKhYmLKHL K12H, R14M K28H, R30M SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence This Clade C consensus synthetic peptide variant from an immunodominant region, differs from the immunodominant Clade B consensus at 2 amino acids (11.1%) and both were recognized by subtype-B-infected subjects. Zhao2007
53201 KK9 31 B     Gag 18 26 p17(18-26) 841..867 A3 KIRLRPGGK KIRLRPGGq K9Q K26Q E, P escape documented in this paper, processing CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay Variant inhibits processing, resulting in rapid decline in the KK9 specific CD8+ T-cell response. Allen2004
55770 KK9 153 B     Gag 18 26 p17(18-26) 841..867 A3 KIRLRPGGK KIRLRPGGr K9R K26R SF susceptible form Flow cytometric T-cell cytokine assay KIRLRPGGK was recognized by 3 patients. The autologous sequence in one patient was KIRLRPGGr which induced high frequency response. Daucher2008
55233   790 B, CRF01_AE   B Gag 18 26 p17(18-26) 841..867 A3 KIRLRPGGK KIRLRPGGr K9R K26R IE inferred escape Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This variant developed in B1 to include 42% of the viruses within 4 years. Kozaczynska2007
53818   1300 A     Gag 18 26 p17(18-26) 841..867 A*0301 KIRLRPGGK KIRLRPGGr K9R K26R DHB diminished HLA binding or increased off-rate CD8 T-cell Elispot - IFNy, HLA binding, Sequence This variant was seen in Donor1 and Recipient1. It was not recognized by either subject and showed diminished binding to HLA. The restricting HLA-A*0301 was only carried in the Donor. Milicic2005
53838 KR9 1570 B     Gag 18 26 p17(18-26) 841..867 A3 KIRLRPGGK KIRLRPGGr K9R K26R LE, OV literature escape, observed variant Sequence This variant from the HXB2 sequence was present in the restricting HLA-A3 allele carrying mother, M-1001, as well as her HLA-A*31-carrying infant, P-1024. Infant P-1024 had lost this variant by 15 months of age. Sanchez-Merino2005
5   1838       Gag 18 26 p17(18-26) 841..867 A3 KIRLRPGGK KIRLRPGGr K9R K26R E escape documented in this paper Chromium-release assay This escape was not recognized by HIV-transmitting mothers Wilson1999a
5   1839       Gag 18 26 p17(18-26) 841..867 A3 KIRLRPGGK rIRLRPGGr K1R, K9R K18R, K26R E escape documented in this paper Chromium-release assay This escape was not recognized by HIV-transmitting mothers Wilson1999a
52827 A3-KK9 Gag 2281 B     Gag 18 26 p17(18-26) 841..867 B7 KIRLRPGGK{*R} KIRLRPGGK{*t} R+2T R28T E, P escape documented in this paper, processing CD8 T-cell Elispot - IFNy Response declined over time; authors suggested that the decline was due to a downstream Arg -> Thr substitution at C+2 that may impair processing. Altfeld2002a
55233   2325 B, CRF01_AE   B Gag 18 26 p17(18-26) 841..867 A3 KIRLRPGGK{KS} KIRLRPGGK{Kr} S+2R S28R OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in B2. Kozaczynska2007
53629   113       Gag 19 27 p17(19-27) 844..870 B27 IRLRPGGKK IRLRPGGrK K8R K26R SF susceptible form Flow cytometric T-cell cytokine assay, Intracellular cytokine staining The dominant viral sequence was irlrpggRk, found in 12/15 clones, while the screening sequence IRLRPGGKK was found in 3/15 clones. The least frequent variant stimulated the strongest response. Casazza2005a
1819 IK9 385       Gag 19 27 p17(19-27) 844..870 B27 IRLRPGGKK IRLRPGrKK G7R G25R OV observed variant   Variant found in one B27 positive child in 4/11 clones, but not in its B27 positive mother Goulder2001c
1819 IK9 386       Gag 19 27 p17(19-27) 844..870 B27 IRLRPGGKK IRLRPrrKK G6R, G7R G24R, G25R OV observed variant   Variant found in one B27 positive child in 1/11 clones, but not in its B27 positive mother Goulder2001c
1819 IK9 387       Gag 19 27 p17(19-27) 844..870 B27 IRLRPGGKK IRkRPGGKK L3K L21K OV observed variant   Variant found in one B27 positive child in 1/19 clones, but not in its B27 positive mother Goulder2001c
1819 IK9 388       Gag 19 27 p17(19-27) 844..870 B27 IRLRPGGKK IRLgPGGsK R4G, K8S R22G, K26S IE inferred escape   Author tabulates this variant found in one B27 positive child in 1/8 clones, and in its B27 positive mother in 1/10 clones as an escape variant. Goulder2001c
1819 IK9 389       Gag 19 27 p17(19-27) 844..870 B27 IRLRPGGKK IRLRPGGsK K8S K26S IE inferred escape   Variant found in one B27 positive child in 7/8 clones, and in its B27 positive mother in 9/10 clones. Goulder2001c
53202 RK9 32 B     Gag 20 28 p17(20-28) 847..873 A3 RLRPGGKKK RLRPGGKqK K8Q K27Q E escape documented in this paper CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay Variant abrogates the response. Allen2004
52824 A3-RK9 Ga9 43 B     Gag 20 28 p17(20-28) 847..873 A3 RLRPGGKKK RLRPGGKKt K9T K28T DR diminished response CD8 T-cell Elispot - IFNy Superinfection. The second infecting strain had the variant rlrpggkkT. The CTL response declined over time, and the response to the second variant was lower than to the first one Altfeld2002a
53602 RK9 59 B     Gag 20 28 p17(20-28) 847..873 A*0301 RLRPGGKKK RLRPGGKKq K9Q K28Q E escape documented in this paper CD8 T-cell Elispot - IFNy, Chromium-release assay, Intracellular cytokine staining Drastically reduced avidity. The response to this peptide was not apparent until month 20, by month 32 the escape variant was present. Bansal2005a
23   98   A, B, D C Gag 20 28 p17(20-28) 847..873 A3 RLRPGGKKK RLRPGGKKh K9H K28H SSF subtype-specific susceptible form Chromium-release assay The consensus peptide of C clade viruses is RLRPGGKKh and is equally reactive. Cao1997a
53633   114       Gag 20 28 p17(20-28) 847..873 A3, A30, B42, B62 RLRPGGKKK RLRPGGKKq K9Q K28Q DR, SF diminished response, susceptible form Flow cytometric T-cell cytokine assay, Intracellular cytokine staining The majority of viral sequences prior to therapy were rlrpggkkQ. At week 14 of therapy a major change in the viral quasispecies occurred: the variants present were found to be rlrpggkkK (14/16 clones) and rlrpggkkR (2/16 clones), both well recognized by HIV-specific CD8 T cells. At week 19, the quasispecies reverted back to the less well-recognized rlrpggkkQ variant. Casazza2005a
53633   115       Gag 20 28 p17(20-28) 847..873 A3, A30, B42, B62 RLRPGGKKK RLRPGGKKr K9R K28R SF susceptible form Flow cytometric T-cell cytokine assay, Intracellular cytokine staining The majority of viral sequences prior to therapy were rlrpggkkQ. At week 14 of therapy a major change in the viral quasispecies occurred: the variants present were found to be rlrpggkkK (14/16 clones) and rlrpggkkR (2/16 clones), both well recognized by HIV-specific CD8 T cells. At week 19, the quasispecies reverted back to the less well-recognized rlrpggkkQ variant. Casazza2005a
56296 RK9 154 B     Gag 20 28 p17(20-28) 847..873 A3, B7 RLRPGGKKK RLRPGGrKr K7R, K9R K26R, K28R SF susceptible form Flow cytometric T-cell cytokine assay RLRPGGKKK was recognized by 3 patients. One patient had variants RLRPGGrKr and RLRPGGKKr, which were well recognized within longer peptides. Daucher2008
56296 RK9 155 B     Gag 20 28 p17(20-28) 847..873 A3, B7 RLRPGGKKK RLRPGGKKr K9R K28R SF susceptible form Flow cytometric T-cell cytokine assay RLRPGGKKK was recognized by 3 patients. One patient had variants RLRPGGrKr and RLRPGGKKr, which were well recognized within longer peptides. Daucher2008
52994   305       Gag 20 28 p17(20-28) 847..873 A3 RLRPGGKKK RLRPGGKKr K9R K28R SF susceptible form   The variant became fixed in the viral population at 20 months post-seroconversion. CTL responses to both wild type and variant peptides were detectable and decreased over time, then increased after mutation fixation. Geels2003
18   357       Gag 20 28 p17(20-28) 847..873 A*03 RLRPGGKKK RLRPGGKKc K9C K28C E escape documented in this paper Chromium-release assay HLA-identical siblings infected with the same batch. One responded to RLRPGGKKK, the non-responder carried RLRPGGKKc. There was no CTL response to this variant and the variant was not recognized by CTLs. Goulder1997Goulder1997e
54533 RK9 1020 B B C Gag 20 28 p17(20-28) 847..873 A3 RLRPGGKKK RLRPGGKKh K9H K28H DR diminished response CD8 T-cell Elispot - IFNy Cross-recognition of the variant is seen with both C- and A-clades. The C-clade variant contains a change at position 9 to RLRPGGKKh. Typically, magnitude and avidity of binding for T-cell responses were much lower to the C-clade variant. Malhotra2007
53817   1301 A     Gag 20 28 p17(20-28) 847..873 A*0301 RLRPGGKKK RLRPGGrKK K7R K26R OV observed variant CD8 T-cell Elispot - IFNy, HLA binding, Sequence This K26R variant was found in both Donor1 and Recipient1. The restricting HLA-A*0301 was only carried in the Donor. Milicic2005
53817   1302 A     Gag 20 28 p17(20-28) 847..873 A*0301 RLRPGGKKK RLRPGGrKt K7R, K9T K26R, K28T E escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding, Sequence Donor1 who carried the restricting HLA-A*0301 generated this mutation which rose to fixation and was not recognized. It was not found in Recipient1 as the mutation arose after transmission of virus between the pair. Milicic2005
53817   1303 A     Gag 20 28 p17(20-28) 847..873 A*0301 RLRPGGKKK RLRPGGKKq K9Q K28Q DHB, E diminished HLA binding or increased off-rate, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding, Sequence This K28Q variant was seen in Donor2 and Recipient2, where only the donor carried the restricting allele. It was not recognized and binding to HLA was abrogated in the Donor. Milicic2005
58244   2835 B B B Gag 20 28 p17(20-28) 847..873 A*0301 {KWEKI}RLRPGGKKK {rWEKI}RLRPGGKKK K-5R K15R IE inferred escape Sequence 3/16 and 1/11 sequences of peptide {KWEKI}RLRPGGKKK varied at 639 and 821 DFOSx to {rWEKI}RLRPGGKKK. Position 15 in the peptide is marked as being under selection to vary. Ferrari2011
53748 RY10 752 B     Gag 20 29 p17(20-29) 847..876 B62 RLRPGGKKKY RLRPGGrKKY K7R K26R SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay Variant was detected over a 5 year time period in a patient. The variant was better recognized than the wt epitope by patient CTLs. Koibuchi2005a
53839 RY10 1571       Gag 20 29 p17(20-29) 847..876 A30 RLRPGGKKKY RLRPGGKKqY K9Q K28Q DR diminished response CD8 T-cell Elispot - IFNy, Sequence This variant from the HXB2 sequence was present in the restricting HLA-A30 allele carrying mother, M-1003, as well as her non-HLA-A30-carrying infant, P-1189. Decreased recognition of the variant was seen relative to index epitope. This variant was still detected at 12 months of age in Infant P-1189. Sanchez-Merino2005
53839 RY10 1572       Gag 20 29 p17(20-29) 847..876 A30 RLRPGGKKKY RLRPGGKKrY K9R K28R DR diminished response CD8 T-cell Elispot - IFNy, Sequence This variant from the HXB2 sequence was present in the restricting HLA-A30 allele carrying mother, M-1002, as well as her HLA-A30-carrying infant, P-1031. Decreased recognition of the variant was seen relative to index epitope in the mother. The variant was detected at decreasing frequencies by 11 months of age in infant P-1031, but recognition was equivalent to index epitope recognition in the infant. Sanchez-Merino2005
57682 EnvRY10 2678 A, B, C, D A, B, C, D B, C Gag 20 29 p17(20-29) 847..876 A3 RLRPGGKKKY RLRPGGKKhY K9H K28H SF, SSF susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Intracellular cytokine staining Variant RLRPGGKKhY was found at frequencies of 2 and 48 in clades B and C respectively. Koup2010
57682 EnvRY10 2679 A, B, C, D A, B, C, D B, C Gag 20 29 p17(20-29) 847..876 A3 RLRPGGKKKY RLRPGGKKrY K9R K28R SF, SSF susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Intracellular cytokine staining Variant RLRPGGKKrY was found at frequencies of 9 and 14 in clades B and C respectively. Koup2010
57682 EnvRY10 2680 A, B, C, D A, B, C, D A, B, C, D Gag 20 29 p17(20-29) 847..876 A3 RLRPGGKKKY RLRPGGKKqY K9Q K28Q SF, SSF susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Intracellular cytokine staining Variant RLRPGGKKqY was found at frequencies of 5, 11, 8 and 5 in clades A, B, C and D respectively. Koup2010
57682 EnvRY10 2681 A, B, C, D A, B, C, D D Gag 20 29 p17(20-29) 847..876 A3 RLRPGGKKKY qLRPGGKKrY R1Q, K9R R20Q, K28R SF, SSF susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Intracellular cytokine staining Variant qLRPGGKKrY was found at a frequency of 23 in clade D. Koup2010
57875   2944 C C C Gag 20 29 p17(20-29) 847..876 B*4201 RLRPGGKKHY kLRPGGKKHY R1K R20K IE inferred escape Sequence Subject CAP 274 carried this escape in 9/9 sequences 2.4 months post-infection (Mo.PI) and in 7/7 sequences 5.1 Mo.PI. Chopera2011
57875   2945 C C C Gag 20 29 p17(20-29) 847..876 B*4201 RLRPGGKKHY kLRPGGKKrY R1K, H9R R20K, H28R IE inferred escape Sequence Subject CAP 274 carried this escape in 19/19 sequences 13.9 months post-infection. Chopera2011
57875   2946 C C C Gag 20 29 p17(20-29) 847..876 B*4201 RLRPGGKKHY RLRPGGKKrY H9R H28R IE inferred escape Sequence Subject CAP 239 carried this escape in 4/9 sequences 18.2 months post-infection. Chopera2011
57875   2947 C C C Gag 20 29 p17(20-29) 847..876 B*4201 RLRPGGKKHY RLRPGGKKqY H9Q H28Q IE inferred escape Sequence Subject CAP 239 carried this escape in 5/9 sequences 18.2 months post-infection. Chopera2011
55629   12 A, CRF02_AG, CRF01_AE AG A, AE Gag 20 31 p17(20-31) 847..882   RLRPGGKKRYRL RLRPGGKKkYRL R9K R28K SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy 1 subject responded to peptide RLRPGGKKRYRL from subtype CRF02_AG and to peptide RLRPGGKKkYRL from subtypes A and CRF01_AE. Aidoo2008
53611   63 A, D     Gag 21 35 p17(21-35) 850..894   LRPGGKKKYRLKHLV LRPGGKKKYkLKHLV R10K R30K OV observed variant CD8 T-cell Elispot - IFNy The sequence contains a known B8 epitope, but the subjects recognizing it were B8-negative. The autologous viral sequence was lrpggkkkyKlkhlv, and the index peptide was recognized. Barugahare2005
57700   2594       Gag 21 35 p17(21-35) 850..894 B*08 LRPGGKKKYKLKHIV LRPGGKKqYKLKHIV K8Q K28Q SF susceptible form CD8 T-cell Elispot - IFNy CTL response to variant LRPGGKKqYKLKHIV was also detected 48 weeks after TI began. Schweighardt2010
57722   2620       Gag 21 35 p17(21-35) 850..894   LRPGGKKKYKLKHIV LRPGGKKrYKLKHIV K8R K28R SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant LRPGGKKrYKLKHIV is seen in patient I04. Vollbrecht2010
57722   2621       Gag 21 35 p17(21-35) 850..894   LRPGGKKKYKLKHIV LRPGGKKKYrLKHlV I14L, K6R I34L, K26R SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant LRPGGrKKYKLKHlV is seen in patient I04. Vollbrecht2010
57722   2622       Gag 21 35 p17(21-35) 850..894   LRPGGKKKYKLKHIV LRPGGKKKYrLKHIV K10R K30R SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant LRPGGKKKYrLKHIV is seen in patient C06. Vollbrecht2010
36   170 A A B Gag 21 40 p17(21-40) 850..909 Cw4 LRPGGKKKYRLKHLVWASRE LRPGGKKKYkLKHiVWASRE R10K, L14I R30K, L34I SNSF subtype-specific non-susceptible form   CTL responses in three individuals with non-clade B infections were studied, 2 with subtype A infections, 1 with subtype C -- their infections all originated in East Africa. This epitope was defined in an A subtype infection -- the B clade variant (LRPGGKKKYKLKHIVWASRE) has two mutations relative to the A subtype form, and the CTLs from this patient were not A-B cross-reactive. Dorrell1999
54602   337 A, C, D C D Gag 22 29 p17(22-29) 853..876 B42, B7 RPGGKKHY RPGGKKkY H7K H28K DR diminished response   The wild type epitope sequence was a subtype C peptide, the variant found in subtype D. CTL response in 56 individuals from Tanzania was strongest for subtype D peptide, and lower for subtype C, due to point mutation effect. Geldmacher2007
54602   338 A, C, D C A Gag 22 29 p17(22-29) 853..876 B42, B7 RPGGKKHY RPGGKKqY H7Q H28Q DR diminished response   The wild type epitope sequence was a subtype C peptide, the variant found in subtype A. CTL response in 56 individuals from Tanzania was strongest for subtype D peptide, and lower for subtype A, due to point mutation effect. Geldmacher2007
56297   156 B     Gag 22 30 p17(22-30) 853..879 B7 RPGGKKKKYK RPGGrKKrYK K5R, K8R K26R, K29R SF susceptible form Flow cytometric T-cell cytokine assay RPGGKKKKYK was recognized by 3 patients. One patient had variants RPGGrKKrYK, RPGGKKKrYK, RPGGKKKKYr which were well recognized. Variant RPGGKKKKYr was also present and recognized in other 2 patients Daucher2008
56297   157 B     Gag 22 30 p17(22-30) 853..879 B7 RPGGKKKKYK RPGGKKKrYK K8R K29R SF susceptible form Flow cytometric T-cell cytokine assay RPGGKKKKYK was recognized by 3 patients. One patient had variants RPGGrKKrYK, RPGGKKKrYK, RPGGKKKKYr which were well recognized. Variant RPGGKKKKYr was also present and recognized in other 2 patients Daucher2008
56297   158 B     Gag 22 30 p17(22-30) 853..879 B7 RPGGKKKKYK RPGGKKKKYr K10R K31R SF susceptible form Flow cytometric T-cell cytokine assay RPGGKKKKYK was recognized by 3 patients. One patient had variants RPGGrKKrYK, RPGGKKKrYK, RPGGKKKKYr which were well recognized. Variant RPGGKKKKYr was also present and recognized in other 2 patients Daucher2008
58700 p17-RM9 3110 C C C Gag 22 30 p17(22-30) 853..879 B*4201, B*4202 RPGGKKHYM RPGGKKrYM H7R H28R E escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding, Sequence p17-RM9 mutation, RPGGKKrYM, is selected in 13% HLA-B*4201 (8% have wt RM9), 10% HLA-B*4202 (31% have wt RM9) and 8% on-HLA-B*42 (46% have wt RM9) subjects. The authors designate this variant as an escape when presented by HLAs-B*4201 and -B*4202. Kloverpris2012a
58700 p17-RM9 3111 C C C Gag 22 30 p17(22-30) 853..879 B*4201, B*4202 RPGGKKHYM RPGGKKHYk M9K M30K OV observed variant CD8 T-cell Elispot - IFNy, HLA binding, Sequence p17-RM9 mutation, RPGGKKHYk, is selected in 9% HLA-B*4201 (8% have wt RM9), 5% HLA-B*4202 (31% have wt RM9) and 2% on-HLA-B*42 (46% have wt RM9) subjects. Kloverpris2012a
58700 p17-RM9 3112 C C C Gag 22 30 p17(22-30) 853..879 B*4201, B*4202 RPGGKKHYM RPGGKKHYr M9R M30R OV observed variant CD8 T-cell Elispot - IFNy, HLA binding, Sequence p17-RM9 mutation, RPGGKKHYr, is selected in 4% HLA-B*4201 (8% have wt RM9), 0% HLA-B*4202 (31% have wt RM9) and 1% on-HLA-B*42 (46% have wt RM9) subjects. Kloverpris2012a
53687   326 B, D     Gag 22 31 p17(22-31) 853..882 Cw4 RPGGKKKYKL RPGGnKKYKL K5N K26N OV observed variant   Cross-clade T cell responses are frequently induced in individuals infected with different HIV-1 clades. There was an inverse correlation between the height of responses and epitope sequence divergence. For Gag epitopes, the magnitude of the response was directly linked to the homology between HLA anchor residues. Geels2005
55633   13 A, CRF02_AG AG A Gag 23 34 p17(23-34) 856..891   PGGKKRYRLKHL PGGKKkYRLKHL R6K R28K SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy 1 subject responded to peptide PGGKKRYRLKHL from subtype CRF02_AG and to peptide PGGKKkYRLKHL from subtype A. Aidoo2008
53683   327 B, D     Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGKKKYKm L8M L31M OV observed variant   Cross-clade T cell responses are frequently induced in individuals infected with different HIV-1 clades. There was an inverse correlation between the height of responses and epitope sequence divergence. For Gag epitopes, the magnitude of the response was directly linked to the homology between HLA anchor residues. Geels2005
54627 GL8 954 B     Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGKKKYKf L8F L31F E escape documented in this paper CD8 T-cell Elispot - IFNy Presumed escape variant was transmitted from a B8 positive donor to a B8 negative recipient. The variant was not recognized by CTLs. Liu2006
38   1104   B   Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGKKKYrL K7R K30R SNSF subtype-specific non-susceptible form Chromium-release assay This circulating Ugandan variant was not recognized by a CTL clone from a patient infected with Clade B virus. McAdam1998
38   1105   B   Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGnKrYrL K3N, K5R, K7R K26N, K28R, K30R SNSF subtype-specific non-susceptible form Chromium-release assay A peptide containing this circulating Ugandan variant was not recognized by a CTL clone from a Clade B-infected patient. McAdam1998
38   1106   B   Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGKKKYqL K7Q K30Q SNSF subtype-specific non-susceptible form Chromium-release assay A peptide containing this circulating Ugandan variant was not recognized by a CTL clone from a Clade B-infected patient. McAdam1998
38   1107   B   Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGKKKYrm K7R, L8M K30R, L31M SNSF subtype-specific non-susceptible form Chromium-release assay A peptide containing this circulating Ugandan variant was not recognized by a CTL clone from a Clade B-infected patient. McAdam1998
38   1108   B   Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGsKKYKL K3S K26S SNSF subtype-specific non-susceptible form Chromium-release assay A peptide containing this circulating Ugandan variant was not recognized by a CTL clone from a Clade B-infected patient. McAdam1998
38   1109   B   Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGKKtYqL K5T, K7Q K28T, K30Q SNSF subtype-specific non-susceptible form Chromium-release assay A peptide containing this circulating Ugandan variant was not recognized by a CTL clone from a Clade B-infected patient. McAdam1998
53819 GL8 1304 A     Gag 24 31 p17(24-31) 859..882 B*0801 GGKKKYKL GGrKKYKL K3R K26R E escape documented in this paper CD8 T-cell Elispot - IFNy, Sequence This variant was seen in Donor1 and Recipient1, where only the donor carried the restricting HLA-B*0801 allele. It was not recognized by either subject. Milicic2005
53819 GL8 1305 A     Gag 24 31 p17(24-31) 859..882 B*0801 GGKKKYKL GGKKqYrL K5Q, K7R K28Q, K30R DHB, E diminished HLA binding or increased off-rate, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding, Sequence This anchor residue variant was seen in Donor2 and Recipient2, both of whom carried the restricting HLA-B*0801 allele. It was not recognized and binding to HLA was greatly reduced. Milicic2005
40   1440 B B B Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGKKqYKL K5Q K28Q E escape documented in this paper Chromium-release assay, HLA binding This variant from the index was seen from the earliest recorded time point. It is either an escape that became fixed or infection occurred with the virus bearing variant Q5. Diminished recognition by index epitope-specific CTL was measured. Price1997
40   1441 B B B Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL erKKqYKL G1E, G2R, K5Q G24E, G25R, K28Q OV observed variant   This variant from the index epitope was seen at the earliest recorded time point but was later lost. Price1997
53840 GL8 1573 B     Gag 24 31 p17(24-31) 859..882 B8 GGKKKYKL GGrKKYKL K3R K26R R reversion CD8 T-cell Elispot - IFNy, Sequence This variant from the HXB2 sequence was present in the restricting HLA-B8 allele carrying mother, M-1001, as well as her non-HLA-B8-carrying infant, P-1024. Infant P-1024 had lost this variant by 15 months of age. Sanchez-Merino2005
46   1344       Gag 24 32 p17(24-32) 859..885 B8 GGKKKYKLK GGrKKYKLK K3R K26R E, SF escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, HLA binding, Longitudinal study Both K and R variants bind HLA-B8. The predominant variant shifts from K to R, back to K. R variant is never recognized; but the K variant is initially recognized, loses recognition and begins to gain recognition by CTL again. Nowak1995
49   373       Gag 24 35 p17(24-35) 859..894 B8 GGKKKYKLKHIV GGKKKYKLKHIi V12I V35I SF susceptible form   This variant was recognized as efficiently as the wt epitope by patient CTLs. Goulder1997ePhillips1991
49   374       Gag 24 35 p17(24-35) 859..894 B8 GGKKKYKLKHIV GrKKKYKLKHIV G2R G25R E escape documented in this paper   This variant failed to be recognized by CTLs and failed to induce target specific lysis. Goulder1997ePhillips1991
49   375       Gag 24 35 p17(24-35) 859..894 B8 GGKKKYKLKHIV GrKKKYKfKHIV G2R, L8F G25R, L31F E escape documented in this paper   This variant failed to be recognized by CTLs and failed to induce target specific lysis. Goulder1997ePhillips1991
49   376       Gag 24 35 p17(24-35) 859..894 B8 GGKKKYKLKHIV rGKKrYKLKHIV G1R, K5R G24R, K28R OV observed variant   Previously published variants of this epitope. Goulder1997ePhillips1991
49   377       Gag 24 35 p17(24-35) 859..894 B8 GGKKKYKLKHIV GGKKqYrLKHIV K5Q, K7R K28Q, K30R OV observed variant   Previously published variants of this epitope. Goulder1997ePhillips1991
49   378       Gag 24 35 p17(24-35) 859..894 B8 GGKKKYKLKHIV GGKKKYqLKHIV K7Q K30Q OV observed variant   Previously published variants of this epitope. Goulder1997ePhillips1991
49   379       Gag 24 35 p17(24-35) 859..894 B8 GGKKKYKLKHIV GGKKKYaLKHli I11L, V12I, K7A I34L, V35I, K30A OV observed variant   Previously published variants of this epitope. Goulder1997ePhillips1991
58382 Peptide 7 2899 C C C Gag 26 40 p17(26-40) 865..909   KKHYMLKHIVWASRE KKHYMLKHlVWASRE I9L I34L SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Chinese Clade-C peptide 7, KKHYMLKHlVWASRE, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58382 Peptide 7 2900 C C B Gag 26 40 p17(26-40) 865..909   xKKHYMLKHIVWASRE gKKkYkLKHlVWASR x1G, I10L, H4K, M6K x26G, I35L, H29K, M31K SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-B peptide 7, gKKkYkLKHlVWASR, did not cross react to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58382 Peptide 7 2903 C C A Gag 26 40 p17(26-40) 865..909   KKHYMLKHIVWASRE KKkYrLKHlVWASRE H3K, M5R, I9L H28K, M30R, I34L SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-A peptide 7, KKkYrLKHlVWASRE, did not cross react to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58382 Peptide 7 2904 C C D Gag 26 40 p17(26-40) 865..909   KKHYMLKHIVWASRE KKkYrLKHlVWASRE H3K, M5R, I9L H28K, M30R, I34L SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-D peptide 7, KKkYrLKHlVWASRE, did not cross react to elicit a response from South African subjects carrying clade-C virus. Zembe2011
1756   87 CRF01_AE B CRF01_AE Gag 28 36 p17(28-36) 871..897 A24 KYKLKHIVW KYKmKHlVW L4M, I7L L31M, I34L SNSF subtype-specific non-susceptible form Chromium-release assay, HLA binding The HLA-A24 subjects tested did not recognize the E clade version KYKmKHlVW, which differs from the previously defined B clade version KYKLKHIVW by two amino acids. Bond2001
54596   339 A, C C D Gag 28 36 p17(28-36) 871..897 A*2301 HYMLKHIVW kYrLKHlVW H1K, M3R, I7L H28K, M30R, I34L DR diminished response   The wild type epitope sequence was a subtype C peptide, the variant found in subtype D. CTL response in 56 individuals from Tanzania was strongest for subtype C peptide, and lower for subtype D, due to point mutation effect. Geldmacher2007
54596   340 A, C C A Gag 28 36 p17(28-36) 871..897 A*2301 HYMLKHIVW qYrmKHlVW H1Q, M3R, L4M, I7L H28Q, M30R, L31M, I34L DR diminished response   The wild type epitope sequence was a subtype C peptide, the variant found in subtype A. CTL response in 56 individuals from Tanzania was strongest for subtype C peptide, and lower for subtype A, due to point mutation effect. Geldmacher2007
53841 QW9 1574       Gag 28 36 p17(28-36) 871..897 A24 KYKLKHIVW qYKLKHIVW K1Q K28Q E, LE escape documented in this paper, literature escape CD8 T-cell Elispot - IFNy, Sequence This variant from the HXB2 sequence was present in the restricting HLA-A24 allele carrying mother, M-1003, as well as her HLA-A24-carrying infant, P-1189. Decreased recognition of the variant was seen relative to wild type index epitope. This variant was still detected at 12 months of age in infant P-1189. While the mother could recognize index epitope QW9, but not this variant, infant P-1189 could not recognize either index or variant. Sanchez-Merino2005
53158   1877       Gag 28 36 p17(28-36) 871..897 A24 KYKLKHIVW KYrLKHlVW K3R, I7L K30R, I34L E, P, SF escape documented in this paper, processing, susceptible form Chromium-release assay This 3R variant escaped from killing by Gag-epitope-specific CTL clonal lines when presented as an endogenously expressed sequence on transformed cells, but was recognized when exogenously loaded as synthetic peptide. A processing or epitope presentation mutation is assumed. Only 1/8 screened A24-positive individuals had CTL activity against this mutant. Yokomaku2004
53158   1879       Gag 28 36 p17(28-36) 871..897 A24 KYKLKHIVW qYKLKHIVW K1Q K28Q E, P, SF escape documented in this paper, processing, susceptible form Chromium-release assay This variant escaped from killing by Gag-epitope-specific CTL clonal lines when presented as an endogenously expressed sequence on transformed cells, but was recognized when exogenously loaded as synthetic peptide. A processing or epitope presentation mutation is assumed. Yokomaku2004
53158   1880       Gag 28 36 p17(28-36) 871..897 A24 KYKLKHIVW rYrLKHlVW K1R, K3R, I7L K28R, K30R, I34L E, P, SF escape documented in this paper, processing, susceptible form Chromium-release assay This variant escaped from killing by Gag-epitope-specific CTL clonal lines when presented as an endogenously expressed sequence on transformed cells, but was recognized when exogenously loaded as synthetic peptide. A processing or epitope presentation mutation is assumed. Yokomaku2004
55928 KW9(p17) 1904 B B B Gag 28 36 p17(28-36) 871..897   KYRLKHLVW KYkLKHLVW R3K R30K OV observed variant CD8 T-cell Elispot - IFNy, Sequence This Asian B Clade optimal epitope differs from the consensus B at one position. It is predicted to be HLA-A24 restricted. Experimentally, B clade consensus peptide was used to challenge CTL response in subjects commonly carrying the Asian B-type epitope. Zhai2008
57701   2595       Gag 28 36 p17(28-36) 871..897 A*23 KYKLKHIVW qYKLKHIVW K1Q K28Q SF susceptible form CD8 T-cell Elispot - IFNy Gag variant qYKLKHIVW also elicited CTL response 48 weeks after start of TI in Patient 311. Schweighardt2010
58187 Gag28-36 2782 B B B Gag 28 36 p17(28-36) 871..897 A*2402 KYKLKHIVW KYrLKHIVW K3R K30R EL, LE epitope loss, literature escape CD8 T-cell Elispot - IFNy, Chromium-release assay, Intracellular cytokine staining, Relative replication capacity assay, Tetramer binding This K3R mutant was used for studies comparing CTL specific for mutants and WT KYKLKHIVW. The 3R mutant was unable to revert to WT in HLA-A*2402 minus subjects. Akahoshi2012
58383 Peptide 11 2905 C C B Gag 42 56 p17(42-56) 913..957   xERFALNPGLLETSE lERFAvNPGLLETSE x1L, L6V x42L, L47V SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-B peptide 11, lERFAvNPGLLETSE, did not cross react to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58383 Peptide 11 2906 C C A Gag 42 56 p17(42-56) 913..957   ERFALNPGLLETSEG ERFALNPsLLETaEG S13A, G8S S54A, G49S SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-A peptide 11, ERFALNPsLLETaEG, did not cross react to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58384 Peptide 15 2907 C C C Gag 58 72 p17(58-72) 961..1005   KQIMKQLQPALQTGT KQIiKQLQPALQTGT M4I M61I SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Chinese Clade-C peptide 15, KQIiKQLQPALQTGT, did not cross react to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58384 Peptide 15 2908 C C B Gag 58 72 p17(58-72) 961..1005   xKQIMKQLQPALQTGT crQIlgQLQPALQTGT x1C, K2R, M5L, K6G x58C, K59R, M62L, K63G SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-B peptide 15, crQIlgQLQPALQTGT, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58384 Peptide 15 2909 C C D Gag 58 72 p17(58-72) 961..1005   KQIMKQLQPALQTGT KQIigQLQPAiQTGs L11I, T15S, M4I, K5G L68I, T72S, M61I, K62G SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-D peptide 15, KQIigQLQPAiQTGs, did not cross react to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58384 Peptide 15 2910 C C A Gag 58 72 p17(58-72) 961..1005   xKQIMKQLQPALQTGT cqQImeQLQsALkTse x1C, P10S, Q13K, G15S, T16E, K2Q, K6E x58C, P67S, Q70K, G72S, T73E, K59Q, K63E SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-A peptide 15, cqQImeQLQsALkTse, did not cross react to elicit a response from South African subjects carrying clade-C virus. Zembe2011
53684   328 B     Gag 71 79 p17(71-79) 1000..1026 A1 GSEELRSLY GtEgikSLh S2T, E4G, L5I, R6K, Y9H S72T, E74G, L75I, R76K, Y79H OV observed variant   Cross-clade T cell responses are frequently induced in individuals infected with different HIV-1 clades. There was an inverse correlation between the height of responses and epitope sequence divergence. For Gag epitopes, the magnitude of the response was directly linked to the homology between HLA anchor residues. Geels2005
54577 GY9 627 B     Gag 71 79 p17(71-79) 1000..1026 A*01 GSEELRSLY GSEELRSLf Y9F Y79F E escape documented in this paper   The variant was present in most of the clones by week 139 and was not recognized by the CTLs. Karlsson2007
54577 GY9 628 B     Gag 71 79 p17(71-79) 1000..1026 A*01 GSEELRSLY GSEELRSLc Y9C Y79C IE inferred escape   Author tabulates this minor variant (1/12) found in patient OP428 at week 63 as viral escape. No CTL response. Karlsson2007
53821   1306 B     Gag 71 79 p17(71-79) 1000..1026 A*0101 GSEELRSLY GSEEikSLY L5I, R6K L75I, R76K DHB, E diminished HLA binding or increased off-rate, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding, Sequence This variant was seen in Donor2 and Recipient2, both of whom carried the restricting HLA-A*0101 allele. It was not recognized and binding to HLA was reduced. Milicic2005
53820   1307 A     Gag 71 79 p17(71-79) 1000..1026 A*0101 GTEELRSLY GTEELRSLf Y9F Y79F DHB, E diminished HLA binding or increased off-rate, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding, Sequence This Y79F variant was seen in Donor1 and Recipient1, where only the donor carried the restricting HLA-A*0101 allele. It was not recognized and showed loss of binding to HLA. Milicic2005
57703   2597       Gag 71 79 p17(71-79) 1000..1026 A*01 GSEELKSLY GSEELrSLY K6R K76R SF susceptible form CD8 T-cell Elispot - IFNy Gag variant GSEELrSLY also elicited CTL responses all through TI in Patient 311. Schweighardt2010
53685   329 B     Gag 74 82 p17(74-82) 1009..1035 B8 ELRSLYNTV gikSLhNTV E1G, L2I, R3K, Y6H E74G, L75I, R76K, Y79H OV observed variant   Cross-clade T cell responses are frequently induced in individuals infected with different HIV-1 clades. There was an inverse correlation between the height of responses and epitope sequence divergence. For Gag epitopes, the magnitude of the response was directly linked to the homology between HLA anchor residues. Geels2005
54580 EV9 629 B     Gag 74 82 p17(74-82) 1009..1035 B*08 ELRSLYNTV ELRSLYNTi V9I V82I OV observed variant   A major variant found in one of the patients throughout study period. Karlsson2007
54580 EV9 630 B     Gag 74 82 p17(74-82) 1009..1035 B*08 ELRSLYNTV ELRSLfNTi Y6F, V9I Y79F, V82I OV observed variant   A major variant found in one of the patients throughout study period. Karlsson2007
54580 EV9 631 B     Gag 74 82 p17(74-82) 1009..1035 B*08 ELRSLYNTV ELRSLcNTi Y6C, V9I Y79C, V82I OV observed variant   Minor variant found in one of the patients at week 63. Karlsson2007
54580 EV9 632 B     Gag 74 82 p17(74-82) 1009..1035 B*08 ELRSLYNTV ELRSLYNai T8A, V9I T81A, V82I OV observed variant   Minor variant found in one of the patients at week 39. Karlsson2007
55238   791 B, CRF01_AE   B, CRF01_AE Gag 74 82 p17(74-82) 1009..1035 B8 ELRSLYNTV ELkSLYNTV R3K R76K OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in CRF01_AE and it did not change over time. It was also the infecting variant in B1. Kozaczynska2007
55238   792 B, CRF01_AE   B Gag 74 82 p17(74-82) 1009..1035 B8 ELRSLYNTV ELkSLYNTi R3K, V9I R76K, V82I IE inferred escape Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This variant developed in B1 to include 50% of the viruses within 4 years. Kozaczynska2007
55238   793 B, CRF01_AE   B Gag 74 82 p17(74-82) 1009..1035 B8 ELRSLYNTV ELkSLfNTV R3K, Y6F R76K, Y79F OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in B2. Kozaczynska2007
55238   2257 B, CRF01_AE B B Gag 74 82 p17(74-82) 1009..1035 B8 ELKSLFNTV ELKSLyNTV F6Y F79Y R reversion Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. The B2 variant is epitope ELKSLFNTV and reversion variant ELKSLyNTV developed in B2 to include 67% of the viruses within 3 years. Kozaczynska2007
57702   2601       Gag 74 82 p17(74-82) 1009..1035 B*08 ELKSLYNTV ELrSLYNTV K3R K76R SF susceptible form CD8 T-cell Elispot - IFNy Gag variant ELrSLYNTV also was recognized through TI in Patient 311. Schweighardt2010
58385 Peptide 19 2911 C C C Gag 74 88 p17(74-88) 1009..1053   ELKSLYNTVATLYCV ELrSLfNTVATLYCV K3R, Y6F K76R, Y79F SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Chinese Clade-C peptide 19, ELrSLfNTVATLYCV, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58385 Peptide 19 2912 C C B Gag 74 88 p17(74-88) 1009..1053   xELKSLYNTVATLYCV eELrSLYNTVATLYCV x1E, K4R x74E, K77R SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-B peptide 19, eELrSLYNTVATLYCV, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58385 Peptide 19 2913 C C D Gag 74 88 p17(74-88) 1009..1053   ELKSLYNTVATLYCV ELrSLYNTVATLYCV K3R K76R SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-D peptide 19, ELrSLYNTVATLYCV, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58385 Peptide 19 2914 C C A Gag 74 88 p17(74-88) 1009..1053   LKSLYNTVATLYCVx LKSLfNTVATLYCVH x15H, Y5F x88H, Y78F SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-A peptide 19, LKSLfNTVATLYCVH, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
55946 RY11(p17) 1905 B B B Gag 76 86 p17(76-86) 1015..1047   RSLFNTVATLY RSLyNTVATLY F4Y F79Y OV observed variant CD8 T-cell Elispot - IFNy, Sequence This Asian B Clade optimal epitope differs from the consensus B at one position. Experimentally, B clade consensus peptide was used to challenge CTL response in subjects commonly carrying the Asian B-type epitope. Zhai2008
57877   2948 C C C Gag 76 86 p17(76-86) 1015..1047 A*3002 RSLYNTVATLY kSLYNTVATLY R1K R76K IE inferred escape Sequence Subject CAP270 carried mutation kSLYNTVATLY in 6/6 sequences 1.8 months post-infection (Mo.PI), 7/7 sequences 2.9 Mo.PI, 9/9 sequences 6.6 Mo.PI, 17/29 sequences 13.3 Mo.PI. Chopera2011
57877   2949 C C C Gag 76 86 p17(76-86) 1015..1047 A*3002 RSLYNTVATLY kSLYNTVAvLY R1K, T9V R76K, T84V IE inferred escape Sequence Subject CAP270 carried mutation kSLYNTVAvLY in 12/29 sequences 13.3 months post-infection. Chopera2011
57300 RY11 2973 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY RSLYNTiATLY V7I V82I DR, E diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant RSLYNTiATLY had a large increase in binding to HLA-A*02 in vitro, but it showed a significant decrease in ex-vivo EliSpot responses in 3/3 chronically-infected, untreated patients as compared to wt RY11. The authors designate V82I mutation-containing peptides to be escapes. Tenzer2009
57300 RY11 2974 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY RSLYNTVAvLY T9V T84V DR, E diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant RSLYNTVAvLY bound at the same Kd to HLA-A*02 as to the WT sequence, but EliSpot response in 2/3 chronically-infected, untreated patients was abolished. Slightly diminished response was seen in one patient. The authors designate T84V mutation-containing peptides as escapes. Tenzer2009
57300 RY11 2975 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY RSLYNTiAvLY V7I, T9V V82I, T84V DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant RSLYNTiAvLY did not bind to HLA-A*02 in vitro, and it showed complete abrogation of ex-vivo EliSpot responses in 1/3 chronically-infected, untreated patients; diminished response in another patient; and no change in the third as compared to WT RY11. The authors designate both V82I and T84V mutation-containing peptides to be escapes. Tenzer2009
57300 RY11 2976 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY RSLfNTiATLY Y4F, V7I Y79F, V82I DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant RSLfNTiATLY did not bind to HLA-A*02, and it showed a significant decrease in ex-vivo EliSpot response in 2 chronically-infected, untreated patients, with no changes in 1 patient as compared to WT RY11. The authors designate Y79F or V82I mutation-containing peptides as escapes. Tenzer2009
57300 RY11 2977 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY RSLfNTVATLY Y4F Y79F DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant RSLfNTVATLY did not bind to HLA-A*02 in vitro, and it showed a decrease in ex-vivo EliSpot response in 2/3 chronically-infected, untreated patients as compared to wt RY11. The authors designate Y79F mutation-containing peptides to be escapes. Tenzer2009
57300 RY11 2978 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY RSLfNTVAvLY Y4F, T9V Y79F, T84V DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant RSLfNTVAvLY did not bind to HLA-A*02 in vitro, and it showed a significant decrease in ex-vivo EliSpot response in 1 chronically-infected, untreated patient; abrogation of CTL response in another such patient; with no changes in the third patient when compared to wt RY11. The authors designate Y79F and T84V mutation-containing peptides to be escapes. Tenzer2009
57300 RY11 2979 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY RSLfNTiAvLY Y4F, V7I, T9V Y79F, V82I, T84V DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant RSLfNTiAvLY did not bind to HLA-A*02 in vitro, and it showed a decrease in ex-vivo EliSpot response in 1/3 chronically-infected, untreated patients; with abrogation of CTL response in 1 other patient; and a slight increase for the last patient as compared with WT RY11. The authors designate Y79F, V82I or T84V mutation-containing peptides to be escapes. Tenzer2009
57300 RY11 2980 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY kSLYNTVATLY R1K R76K DHB, DR diminished HLA binding or increased off-rate, diminished response CD8 T-cell Elispot - IFNy, HLA binding Variant kSLfNTiATLY did not bind to HLA-A*02 in vitro, but it showed a decrease in ex-vivo EliSpot response in 2/3 chronically-infected, untreated patients as compared to WT RY11. Tenzer2009
57300 RY11 2981 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY kSLYNTVAvLY R1K, T9V R76K, T84V DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant kSLYNTVAvLY had loss of binding to HLA-A*02 in vitro; and it showed a significant decrease in ex-vivo EliSpot response in 1 chronically-infected, untreated patient, and abrogation of CTL responses in the other 2. Tenzer2009
57300 RY11 2982 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY kSLYNTiATLY R1K, V7I R76K, V82I DR, E diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant kSLYNTiATLY had an increase in binding to HLA-A*02 in vitro; but it showed a significant decrease in EliSpot response in 1 chronically-infected, untreated patient; abrogation of CTL responses in the second patient; and no change in the third when compared to wt RY11. The authors designate V82I mutation-containing peptides to be escapes. Tenzer2009
57300 RY11 2983 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY kSLYNTiAvLY R1K, V7I, T9V R76K, V82I, T84V DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant kSLYNTiAvLY lost binding to HLA-A*02 in vitro; and it showed a significant decrease in ex-vivo EliSpot response in 2 chronically-infected, untreated patients and abrogation of CTL response in the third. The authors designate V82I or T84V mutation-containing peptides as escapes. Tenzer2009
57300 RY11 2984 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY kSLfNTVATLY R1K, Y4F R76K, Y79F DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant kSLfNTVATLY lost binding to HLA-A*02 in vitro; and it showed a significant decrease in ex-vivo EliSpot response in 3/3 chronically-infected, untreated patients. The authors designate Y79F mutation-containing peptides as escapes. Tenzer2009
57300 RY11 2985 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY kSLfNTiATLY R1K, Y4F, V7I R76K, Y79F, V82I DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant kSLfNTiATLY lost binding to HLA-A*02 in vitro; and it showed a significant decrease in ex-vivo EliSpot responses in 3/3 chronically-infected, untreated patients as compared to wt RY11. The authors designate Y79F or V82I mutation-containing peptides as escapes. Tenzer2009
57300 RY11 2986 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY kSLfNTVAvLY R1K, Y4F, T9V R76K, Y79F, T84V DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant kSLfNTVAvLY lost binding to HLA-A*02 in vitro; and it showed a significant decrease in EliSpot response in 2 chronically-infected, untreated patients; and abrogation of CTL response in the third. The authors designate Y79F or T84V mutation-containing peptides as escapes. Tenzer2009
57300 RY11 2987 B B B Gag 76 86 p17(76-86) 1015..1047 A*0201, A*3002 RSLYNTVATLY kSLfNTiAvLY R1K, Y4F, V7I, T9V R76K, Y79F, V82I, T84V DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Variant kSLfNTiAvLY did not bind to HLA-A*02 in vitro, and it showed a decrease in ex-vivo EliSpot response in 1/3 chronically-infected, untreated patients, with abrogation of CTL response in the other 2 patients as compared to WT RY11. The authors designate Y79F, V82I or T84V mutation-containing peptides to be escapes. Tenzer2009
58604 GagRY11 3056       Gag 76 86 p17(76-86) 1015..1047 A*3002 RSLYNTVATLY RSLYNTVATLc Y11C Y86C E escape documented in this paper Cytokine production, Sequence, Tetramer binding 5/5 (100%) sequenced variants showed this escape, RSLYNTVATLc, in subject 0406; 13/15 (86.7%) in subject 2401; and 8/16 (50%) in subject 3902. Mahlokozera2011
58604 GagRY11 3057       Gag 76 86 p17(76-86) 1015..1047 A*3002 RSLYNTVATLY kSLfNTVATLc R1K, Y11C, Y4F R76K, Y86C, Y79F E escape documented in this paper Cytokine production, Sequence, Tetramer binding 1/22 (4.5%) sequenced variants showed this escape, kSLfNTVATLc, in subject 2007; 1/4 (25%) in subject 5506. Mahlokozera2011
58604 GagRY11 3058       Gag 76 86 p17(76-86) 1015..1047 A*3002 RSLYNTVATLY RSLfNTiATLf Y11F, Y4F, V7I Y86F, Y79F, V82I E escape documented in this paper Cytokine production, Sequence, Tetramer binding 12/18 (66.7%) sequenced variants showed this escape, RSLfNTiATLf, in subject 3706. Mahlokozera2011
53603 SL9 60 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTIATL SLYNTIAvL T8V T84V SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Intracellular cytokine staining The response to this peptide was not apparent until month 20, by month 32 a T to V change was dominant, but the slyntiaVl mutant showed comparable avidity. Bansal2005a
55518 SL9 69 A, B, C, D, F, G, K B A, F Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLYNTVAvL T8V T84V SSF subtype-specific susceptible form Chromium-release assay SL9 epitope variants used were SLYNTVATL for clades B/A1/C/D, SLYNTVAVL for clades A2/F1, and SLFNTVATL for clades G/K. Clade B-elicited CTLs recognized epitopes from all other clades when tested by Cr-release. Bennett2008
55518 SL9 70 A, B, C, D, F, G, K B G, K Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLfNTVATL Y3F Y79F SSF subtype-specific susceptible form Chromium-release assay SL9 epitope variants used were SLYNTVATL for clades B/A1/C/D, SLYNTVAVL for clades A2/F1, and SLFNTVATL for clades G/K. Clade B-elicited CTLs recognized epitopes from all other clades when tested by Cr-release. Bennett2008
55763 SL9 76 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay To identify immunogenically optimized epitopes for use in vaccines, mutants of SL9 were tested in transgenic mice. SLYNTVATL and most common mutant, SLfNTVATL, were weakly immunogenic or cross-reactive. 3 mutants, SLYNlVATL, SLfNlVATL and SiYNlVATL were highly immunogenic. Peptide SiYNlVATL with the additional L2I change allowed great cross-reactivity to the consensus. Blondelle2008
55763 SL9 77 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNlVATL T5L T81L SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay To identify immunogenically optimized epitopes for use in vaccines, mutants of SL9 were tested in transgenic mice. SLYNTVATL and most common mutant, SLfNTVATL, were weakly immunogenic or cross-reactive. 3 mutants, SLYNlVATL, SLfNlVATL and SiYNlVATL were highly immunogenic. Peptide SiYNlVATL with the additional L2I change allowed great cross-reactivity to the consensus. Blondelle2008
55763 SL9 78 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNlVATL Y3F, T5L Y79F, T81L SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay To identify immunogenically optimized epitopes for use in vaccines, mutants of SL9 were tested in transgenic mice. SLYNTVATL and most common mutant, SLfNTVATL, were weakly immunogenic or cross-reactive. 3 mutants, SLYNlVATL, SLfNlVATL and SiYNlVATL were highly immunogenic. Peptide SiYNlVATL with the additional L2I change allowed great cross-reactivity to the consensus. Blondelle2008
55763 SL9 79 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SiYNlVATL L2I, T5L L78I, T81L SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay To identify immunogenically optimized epitopes for use in vaccines, mutants of SL9 were tested in transgenic mice. SLYNTVATL and most common mutant, SLfNTVATL, were weakly immunogenic or cross-reactive. 3 mutants, SLYNlVATL, SLfNlVATL and SiYNlVATL were highly immunogenic. Peptide SiYNlVATL with the additional L2I change allowed great cross-reactivity to the consensus. Blondelle2008
64 SL9 97 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVATL Y3F Y79F E, SF escape documented in this paper, susceptible form   The substitution Y79F was an escape mutation because it interfered with CTL recognition by one CTL clone from an A*0201 infected individual, clone 13010.B17, but it was still recognized by another CTL clone, 115.D4. Brander1999a
96 SL9 99   B, C, D A, C Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F SSF subtype-specific susceptible form Chromium-release assay The consensus peptides of B and D clade viruses and some Cs have the sequence SLYNTVATL. The consensus peptide of A, and some C strains is SLFNTVATL, a form that is cross-reactive. Cao1997a
55051   142   A, C A, D Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I SNSF, SSF subtype-specific non-susceptible form, subtype-specific susceptible form   SLYNTVATL within peptide SLYNTVATLYC from A consensus and C isolate was recognized by 5/9 HLA A*0201 carriers from subtype A Kenyan cohort. The variant SLfNTiATL within peptide SLfNTiATLYC from A isolate and peptide SLfNTiATLWC from D isolate was recognized by 3 out 5 subjects that recognized SLYNTVATL and not recognized by 2 subjects. Currier2006
102 SL9 171 A A, C B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLFNTVATL SLyNTVATL F3Y F79Y SNSF subtype-specific non-susceptible form   CTL responses in three individuals with non-clade B infections were studied, 2 with subtype A infections, 1 with subtype C -- their infections all originated in East Africa. This epitope is most commonly SLYNTVATL in B subtype, and CTL from the C subtype infection did not recognize B clade gag or the 3Y form of the epitope, but did recognize the predominant A and C clade form, SLFNTVATL. Dorrell1999
52187 SL9 178 B     Gag 77 85 p17(77-85) 1018..1044   SLYNTVATL SLYNTVAvL T8V T84V SF susceptible form   SLYNTVATL was the only form of the epitope found initially, but three alternate forms eventually appeared: SLYNTVAVL, SLYNTIATL, and most commonly SLYNTIAVL. These distinct forms bind A2, but have distinct abilities to stimulate different T-cell clonotypes. In subject TX7, the observed mutations of SL9 failed to escape overall CTL recognition, presumably because the six T-cell clonotypes allowed a more flexible response. The BV17 T-cell clone recognized SL9 but not SLYNTIAVL, and BV17 became undetectable at week 20 when SLYNTIAVL predominated. Subsequently BV17 became the second most common clone. Douek2002
52187 SL9 179 B     Gag 77 85 p17(77-85) 1018..1044   SLYNTVATL SLYNTiATL V6I V82I E, SF escape documented in this paper, susceptible form   SLYNTVATL was the only form of the epitope found initially, but three alternate forms eventually appeared: SLYNTVAVL, SLYNTIATL, and most commonly SLYNTIAVL. These distinct forms bind A2, but have distinct abilities to stimulate different T-cell clonotypes. In subject TX7, the observed mutations of SL9 failed to escape overall CTL recognition, presumably because the six T-cell clonotypes allowed a more flexible response. The BV17 T-cell clone recognized SL9 but not SLYNTIAVL, and BV17 became undetectable at week 20 when SLYNTIAVL predominated. Subsequently BV17 became the second most common clone. Douek2002
52187 SL9 180 B     Gag 77 85 p17(77-85) 1018..1044   SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V SF susceptible form   SLYNTVATL was the only form of the epitope found initially, but three alternate forms eventually appeared: SLYNTVAVL, SLYNTIATL, and most commonly SLYNTIAVL. These distinct forms bind A2, but have distinct abilities to stimulate different T-cell clonotypes. In subject TX7, the observed mutations of SL9 failed to escape overall CTL recognition, presumably because the six T-cell clonotypes allowed a more flexible response. The BV17 T-cell clone recognized SL9 but not SLYNTIAVL, and BV17 became undetectable at week 20 when SLYNTIAVL predominated. Subsequently BV17 became the second most common clone. Douek2002
55064 SL9 183       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V DR diminished response CD8 T-cell Elispot - IFNy, Intracellular cytokine staining Immune responses were examined in monozygotic male twins infected simultaneously with the same virus. SLYNTVAvL variant arose in one twin and not the other. Response to the variant was diminished. Draenert2006
54597   341 A, C, D C A, D Gag 77 85 p17(77-85) 1018..1044 A2, A68 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I DR diminished response   The wild type epitope sequence was a subtype C peptide, the variant common to subtypes A and D. CTL response in 56 individuals from Tanzania was strongest for subtype C peptide, and lower for subtypes A and D, due to point mutation effect. Geldmacher2007
97 SL9 358       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLhNaVAvL Y3H, T5A, T8V Y79H, T81A, T84V E escape documented in this paper Chromium-release assay HLA-identical siblings infected with the same batch. One responded to SLYNTVATL, the non-responder carried SLhNaVAvL. There was no CTL response to this variant. Goulder1997Goulder1997e
97 SL9 359       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVATL Y3F Y79F E escape documented in this paper Chromium-release assay A subject went to SLYNTVATL responder to non-responder which coincided with a switch to the variant epitope. The variant had poor CTL recognition and there was no peptide-specific CTLs generated upon stimulation of PBMCs. Goulder1997Goulder1997e
97 SL9 360       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V SF susceptible form Chromium-release assay Variant was recognized by CTLs to a similar level as the wt. Goulder1997Goulder1997e
97 SL9 361       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLhNTVATL Y3H Y79H E escape documented in this paper Chromium-release assay Variant was not recognized by CTLs. Goulder1997Goulder1997e
97 SL9 362       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLlNTVATL Y3L Y79L OV observed variant   Variant was found in one epitope responder in 6% of the clones. Goulder1997Goulder1997e
97 SL9 363       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTVAvL T8V T84V OV observed variant   Variant was found in one epitope responder in 10% of the clones. Goulder1997Goulder1997e
97 SL9 364       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiATL V6I V82I OV observed variant   Variant was found in one epitope responder in 9% of the clones. Goulder1997Goulder1997e
97 SL9 365       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLsNTiATL Y3S, V6I Y79S, V82I OV observed variant   Variant was found in one epitope non-responder in 10% of the clones. Goulder1997Goulder1997e
97 SL9 366       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V OV observed variant   Variant was found in two epitope non-responders in 25% and 38% of the clones, respectively. Goulder1997Goulder1997e
1822 SL9 383       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F E escape documented in this paper   The variant was not recognized by autologous CTL in an infected mother. The variant was transmitted both vertically and horizontally. Goulder2001b
1822 SL9 384       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V E escape documented in this paper   A variant found in an infected mother that was vertically transmitted. The wt epitope was not recognized by children's CTLs. Goulder2001b
104 SL9 408       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F SF susceptible form Chromium-release assay No variants were found in the patient, but this synthetic variant was tested against patient CTLs. The variant was recognized by CTLs and induced target specific lysis. Harrer1998
104 SL9 409       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiATL V6I V82I SF susceptible form Chromium-release assay No variants were found in the patient, but this synthetic variant was tested against patient CTLs. The variant was recognized by CTLs and induced target specific lysis. Harrer1998
104 SL9 410       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V SF susceptible form Chromium-release assay No variants were found in the patient, but this synthetic variant was tested against patient CTLs. The variant was recognized by CTLs and induced target specific lysis. Harrer1998
104 SL9 411       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNaVATL T5A T81A SF susceptible form Chromium-release assay No variants were found in the patient, but this synthetic variant was tested against patient CTLs. The variant was recognized by CTLs and induced target specific lysis. Harrer1998
54498 SL9 467       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiATL V6I V82I NSF, SF non-susceptible form, susceptible form   Variant present in 8% of 76 A2+ patients. Bound strongly to HLA-A2 (binding affinity was 94 nM). Was recognized by some A2+ patient's PBMCs and not recognized by others. Iversen2006
54498 SL9 468       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V OV observed variant   Variant present in 4% of A2+ patients. Bound strongly to HLA-A2 (binding affinity was 20 nM). Was not present in the patients tested for EliSpot responses. Iversen2006
54498 SL9 469       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V E escape documented in this paper   Positively selected transition variant present in 5% of A2+ patients. HLA-binding affinity was sufficient to elicit CTL responses. Not well recognized by patient PBMCs. Iversen2006
54498 SL9 470       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F DHB, SF diminished HLA binding or increased off-rate, susceptible form   Positively selected transition variant present in 16% of A2+ patients. HLA-binding affinity was sufficient to elicit CTL responses but was somewhat weaker compared to other variants. Recognized by patient PBMCs. Iversen2006
54498 SL9 471       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I DR diminished response   Transition variant present in 7% of A2+ patients. Intermediate recognition by patient PBMCs. Iversen2006
54498 SL9 472       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiAvL Y3F, V6I, T8V Y79F, V82I, T84V E, TCR escape documented in this paper, TCR related mutation   Positively selected escape variant present in 7% of A2+ patients. HLA-binding affinity was sufficient to elicit CTL responses but the responses were usually weaker than to other variants. Assumed to impair TCR binding. Iversen2006
54498 SL9 473       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLhNaVAvL Y3H, T5A, T8V Y79H, T81A, T84V SF susceptible form   A minor variant found in one patient. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
54498 SL9 474       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V DR diminished response   Positively selected transition variant present in 11% of A2+ patients. HLA-binding affinity was sufficient to elicit CTL responses. Not well recognized by patient PBMCs. Iversen2006
54498 SL9 475       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiAiL V6I, T8I V82I, T84I OV observed variant   A minor variant found in one patient. Iversen2006
54498 SL9 476       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATv Y3F, L9V Y79F, L85V SF susceptible form   A minor variant found in one patient. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
54498 SL9 477       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNaVATL T5A T81A SF susceptible form   A minor variant found in one patient. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
54498 SL9 478       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNlVAvL T5L, T8V T81L, T84V DHB diminished HLA binding or increased off-rate   A minor variant found in one patient. HLA-binding affinity was not sufficient to elicit CTL responses. Iversen2006
54498 SL9 479       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAif T8I, L9F T84I, L85F DHB diminished HLA binding or increased off-rate   A minor variant found in one patient. HLA-binding affinity was not sufficient to elicit CTL responses. Iversen2006
54498 SL9 480       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNaVATL Y3F, T5A Y79F, T81A R, SF reversion, susceptible form   An unusual variant resulting in strong response. This is suggested to be a transient reversion variant. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
54498 SL9 481       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNaVAvL Y3F, T5A, T8V Y79F, T81A, T84V SF susceptible form   A minor variant found in one patient. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
54498 SL9 482       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNmVATL Y3F, T5M Y79F, T81M SF susceptible form   A minor variant found in one patient. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
54498 SL9 483       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVsTL A7S A83S SF susceptible form   Variant described before. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
54498 SL9 484       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTitvL V6I, A7T, T8V V82I, A83T, T84V SF susceptible form   Variant described before. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
54498 SL9 485       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTisvL V6I, A7S, T8V V82I, A83S, T84V SF susceptible form   Variant described before. HLA-binding affinity was sufficient to elicit CTL responses. Iversen2006
53008 SL9 486 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVATL Y3F Y79F DHB, E diminished HLA binding or increased off-rate, escape documented in this paper   This variant was found in one patient and elicited <50% the response to the wt while it elicited strong response in another patient. Likely mechanism of escape was loss of HLA binding. Jamieson2003
53008 SL9 487 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V E, TCR escape documented in this paper, TCR related mutation   This variant was found in two patients and elicited <50% the response to the wt in both patients. Likely mechanism of escape was loss of T cell recognition. Jamieson2003
53008 SL9 488 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTVvTL A7V A83V IE inferred escape   Variant found in one patient. Decline of CTL responses. Jamieson2003
53008 SL9 489 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I IE inferred escape   Variant found in one patient. Decline of CTL responses. Jamieson2003
53008 SL9 490 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V E, TCR escape documented in this paper, TCR related mutation   This variant was found in two patients and elicited <50% the response to the index peptide in both patients. The likely mechanism of escape was loss of T cell recognition. Jamieson2003
53008 SL9 491 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLhNTVAvL Y3H, T8V Y79H, T84V DHB, E diminished HLA binding or increased off-rate, escape documented in this paper   This variant was found in one patient and elicited <25% the response to the wt in two patients. Likely mechanism of escape was loss of HLA binding. Jamieson2003
53008 SL9 492 B     Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTVAvL T8V T84V DHB, E diminished HLA binding or increased off-rate, escape documented in this paper   This variant was found in three patients and elicited <50% the response to the wt in two patients. Likely mechanism of escape was loss of HLA binding. Jamieson2003
53742   500       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F OV observed variant   Two of the subjects carried this variant of the epitope Jansen2005a
53742   501       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiATL V6I V82I OV observed variant   One of the subjects carried this variant of the epitope. Jansen2005a
54497 SL9 596       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAaL T8A T84A SF susceptible form   This synthesized variant was recognized by CTLs from 8/9 individuals. The variant was more immunogenic than the wt, reduced IL-2-mediated activation induced cell death that the wt CTLs were susceptible to, and induced broad response to several SL9 variants. Kan-Mitchell2006
54497 SL9 597       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLYNTVATL S1L S77L SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 6/8 donors. Kan-Mitchell2006
54497 SL9 598       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAsL T8S T84S SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 7/8 donors. Kan-Mitchell2006
54497 SL9 599       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTpATL V6P V82P SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 1/8 donors. Kan-Mitchell2006
54497 SL9 600       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLYNTVAaL S1L, T8A S77L, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 5/8 donors. Kan-Mitchell2006
54497 SL9 601       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLYNTVAsL S1L, T8S S77L, T84S SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 6/8 donors. Kan-Mitchell2006
54497 SL9 602       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLYNTVlTL S1L, A7L S77L, A83L SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 2/8 donors. Kan-Mitchell2006
54497 SL9 603       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTsAaL V6S, T8A V82S, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 3/8 donors. Kan-Mitchell2006
54497 SL9 604       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLYNTpATL S1L, V6P S77L, V82P SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 3/8 donors. Kan-Mitchell2006
54497 SL9 605       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTpAaL V6P, T8A V82P, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 1/8 donors. Kan-Mitchell2006
54497 SL9 606       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTpAsL V6P, T8S V82P, T84S SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 2/8 donors. Kan-Mitchell2006
54497 SL9 607       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLhNwslaL Y3H, T5W, V6S, A7L, T8A Y79H, T81W, V82S, A83L, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 1/8 donors. Kan-Mitchell2006
54497 SL9 608       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLwNwplaL Y3W, T5W, V6P, A7L, T8A Y79W, T81W, V82P, A83L, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 3/8 donors. Kan-Mitchell2006
54497 SL9 609       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLwNwplsL Y3W, T5W, V6P, A7L, T8S Y79W, T81W, V82P, A83L, T84S SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 3/8 donors. Kan-Mitchell2006
54497 SL9 610       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLhNwplaL Y3H, T5W, V6P, A7L, T8A Y79H, T81W, V82P, A83L, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 3/8 donors. Kan-Mitchell2006
54497 SL9 611       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLhNwplsL Y3H, T5W, V6P, A7L, T8S Y79H, T81W, V82P, A83L, T84S SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 3/8 donors. Kan-Mitchell2006
54497 SL9 612       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLwNTslaL S1L, Y3W, V6S, A7L, T8A S77L, Y79W, V82S, A83L, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 3/8 donors. Kan-Mitchell2006
54497 SL9 613       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLwNwslaL S1L, Y3W, T5W, V6S, A7L, T8A S77L, Y79W, T81W, V82S, A83L, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 2/8 donors. Kan-Mitchell2006
54497 SL9 614       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLwNwslsL S1L, Y3W, T5W, V6S, A7L, T8S S77L, Y79W, T81W, V82S, A83L, T84S SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 1/8 donors. Kan-Mitchell2006
54497 SL9 615       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLwNwplaL S1L, Y3W, T5W, V6P, A7L, T8A S77L, Y79W, T81W, V82P, A83L, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 1/8 donors. Kan-Mitchell2006
54497 SL9 616       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLhNwslaL S1L, Y3H, T5W, V6S, A7L, T8A S77L, Y79H, T81W, V82S, A83L, T84A SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 1/8 donors. Kan-Mitchell2006
54497 SL9 617       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL lLhNwplsL S1L, Y3H, T5W, V6P, A7L, T8S S77L, Y79H, T81W, V82P, A83L, T84S SF susceptible form   74 synthesized SL9 variants were tested for recognition by CTLs from 9 HLA-A2+ donors. This variant was one of the 22 recognized by CTLs. It was recognized by CTLs from 1/8 donors. Kan-Mitchell2006
54497 SL9 618       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F E, SF escape documented in this paper, susceptible form   This variant was not recognized by SL9-CTLs from one patient while it was recognized by the T/A-variant CTLs from this patient and by SL9- and T/A-CTLs derived from sister cells from another patient. Kan-Mitchell2006
54497 SL9 619       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V DR, E diminished response, escape documented in this paper   This variant was not recognized by SL9-CTLs from one patient while it was recognized by the T/A-variant CTLs from this patient and by SL9- and T/A-CTLs derived from sister cells from another patient. It was recognized to a lesser extent than the wt. Kan-Mitchell2006
54497 SL9 620       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiAvL Y3F, V6I, T8V Y79F, V82I, T84V E, SF escape documented in this paper, susceptible form   This variant was not recognized by SL9-CTLs from one patient while it was recognized by the T/A-variant CTLs from this patient and by SL9- and T/A-CTLs derived from sister cells from another patient. Kan-Mitchell2006
54497 SL9 621       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiATL V6I V82I DR, SF diminished response, susceptible form   This variant was recognized by SL9-CTLs from one patient while it was recognized to a lesser extent by the T/A-variant CTLs from this patient. It was recognized by SL9- and T/A-CTLs derived from sister cells from another patient. Kan-Mitchell2006
54497 SL9 622       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V DR, SF diminished response, susceptible form   This variant was recognized by SL9-CTLs from one patient while it was recognized to a lesser extent by the T/A-variant CTLs from this patient. It was recognized by SL9- and T/A-CTLs derived from sister cells from another patient. Kan-Mitchell2006
54497 SL9 623       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SvYNTVATL L2V L78V DR, SF diminished response, susceptible form   This variant was recognized by both SL9-CTLs and by the T/A-variant CTLs from this patient, but to somewhat lesser extent than the wt epitope. It was also recognized by SL9- and T/A-CTLs derived from sister cells from another patient. Kan-Mitchell2006
54556 SL9 633 B     Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLYNTiATL V6I V82I SF susceptible form CD8 T-cell Elispot - IFNy A major variant detected by week 39 in one of the patients that induced a CTL response. Karlsson2007
54556 SL9 634 B     Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I DR, E diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy Variant detected by week 63. Lower magnitude responses than wt and V/I mutant. Positive selection. Seen with upstream changes E62G/V/A, where the 62A mutation persisted and is suggested to reduce fitness cost of the Y/F escape mutation. Karlsson2007
54556 SL9 635 B     Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLYNaiATL T5A, V6I T81A, V82I IE inferred escape CD8 T-cell Elispot - IFNy Author tabulates this variant detected in 1/14 clones at week 39 in patients. OP428 as viral escape. No CTL response detected. Karlsson2007
54556 SL9 636 B     Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLcNTiATL Y3C, V6I Y79C, V82I IE inferred escape CD8 T-cell Elispot - IFNy Author tabulates this variant as a viral escape, detected in 1/12 clones at week 63 in patient OP428. No CTL response detected. Karlsson2007
1649   670       Gag 77 85 p17(77-85) 1018..1044 A2 SLFNTVATL SLyNTVATL F3Y F79Y SF susceptible form CD8 T-cell Elispot - IFNy This epitope and the variant were recognized by 22/26 HLA-A2+ infected women but only by 1/10 HIV-exposed, persistently seronegative women (HEPS). Responses to the epitope and the variant were much higher after HIV-1 seroconversion in previous HEPS. Kaul2001a
53755 SL9 753 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I E escape documented in this paper CD8 T-cell Elispot - IFNy, Chromium-release assay Variant was found in the beginning and at the end of a 7 year period in a patient. It was not recognized by patient CTLs. Koibuchi2005a
53755 SL9 754 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiAaL Y3F, V6I, T8A Y79F, V82I, T84A OV observed variant   Variant was found in 1/22 clones at the beginning of a 7 year period in a patient. Koibuchi2005a
53755 SL9 755 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V E escape documented in this paper CD8 T-cell Elispot - IFNy, Chromium-release assay Variant dominated in the middle of a 7 year period in a patient. It was not recognized by patient CTLs. Koibuchi2005a
53755 SL9 756 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfsTVAvL Y3F, N4S, T8V Y79F, N80S, T84V OV observed variant   Variant was found in 1/28 clones at the middle of a 7 year period in a patient. Koibuchi2005a
53755 SL9 757 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVAvp Y3F, T8V, L9P Y79F, T84V, L85P OV observed variant   Variant was found in 1/28 clones at the middle of a 7 year period in a patient. Koibuchi2005a
53755 SL9 758 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiAvL Y3F, V6I, T8V Y79F, V82I, T84V OV observed variant   Variant was found at the end of a 7 year period in a patient. Koibuchi2005a
53386 gag 77-85 1004 B B HIV-2 Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVcvi Y3F, A7C, T8V, L9I Y79F, A83C, T84V, L85I DR, E, SNSF, TCR diminished response, escape documented in this paper, subtype-specific non-susceptible form, TCR related mutation CD8 T-cell Elispot - IFNy Naturally-occurring HIV-2 variant. It was not recognized well by CTLs from four A2+ HIV infected asymptomatic individuals. The variant bound to HLA-A2 with higher affinity than the wt epitope, indicating that the poor CTL recognition was due to inhibition of TCR recognition. Lopes2003
53386 gag 77-85 1005 B B A Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F DR, E, SNSF, TCR diminished response, escape documented in this paper, subtype-specific non-susceptible form, TCR related mutation CD8 T-cell Elispot - IFNy Naturally-occurring clade A variant. It was poorly recognized by CTLs from some of the A2+ HIV infected asymptomatic individuals. The variant bound to HLA-A2 with higher affinity than the wt epitope, indicating that the poor CTL recognition was due to inhibition of TCR recognition. Lopes2003
53386 gag 77-85 1006 B B G Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNaVATL Y3F, T5A Y79F, T81A DR, E, SNSF, TCR diminished response, escape documented in this paper, subtype-specific non-susceptible form, TCR related mutation CD8 T-cell Elispot - IFNy Naturally-occurring clade G variant. It was poorly recognized by CTLs from some of the A2+ HIV infected asymptomatic individuals. The variant bound to HLA-A2 with higher affinity than the wt epitope, indicating that the poor CTL recognition was due to inhibition of TCR recognition. Lopes2003
53386 gag 77-85 1007 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLaNTVATL Y3A Y79A DR, E, TCR diminished response, escape documented in this paper, TCR related mutation CD8 T-cell Elispot - IFNy Artificially synthesized variant. It was poorly recognized by CTLs from some of the A2+ HIV infected asymptomatic individuals. The variant bound to HLA-A2 with higher affinity than the wt epitope, indicating that the poor CTL recognition was due to inhibition of TCR recognition. Lopes2003
53386 gag 77-85 1008 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYaTVATL N4A N80A DR, E, TCR diminished response, escape documented in this paper, TCR related mutation CD8 T-cell Elispot - IFNy Artificially synthesized variant. It was poorly recognized by CTLs from some of the A2+ HIV infected asymptomatic individuals. The variant bound to HLA-A2 with higher affinity than the wt epitope, indicating that the poor CTL recognition was due to inhibition of TCR recognition. Lopes2003
53386 gag 77-85 1009 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNaVATL T5A T81A DR, E, TCR diminished response, escape documented in this paper, TCR related mutation CD8 T-cell Elispot - IFNy Artificially synthesized variant. It was poorly recognized by CTLs from some of the A2+ HIV infected asymptomatic individuals. The variant bound to HLA-A2 with higher affinity than the wt epitope, indicating that the poor CTL recognition was due to inhibition of TCR recognition. Lopes2003
53386 gag 77-85 1010 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTaATL V6A V82A SF susceptible form CD8 T-cell Elispot - IFNy The only artificially synthesized variant that did not abrogate recognition by CTLs from some of the A2+ HIV infected asymptomatic individuals. The variant bound to HLA-A2 with slightly reduced affinity than the wt epitope. Lopes2003
53386 gag 77-85 1011 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAaL T8A T84A DR, E, TCR diminished response, escape documented in this paper, TCR related mutation CD8 T-cell Elispot - IFNy Artificially synthesized variant. It was poorly recognized by CTLs from some of the A2+ HIV infected asymptomatic individuals. The variant bound to HLA-A2 with higher affinity than the wt epitope, indicating that the poor CTL recognition was due to inhibition of TCR recognition. Lopes2003
54495 SL9 1052 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiATL V6I V82I SF susceptible form Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1053 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V SF susceptible form Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1054 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V SF susceptible form Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1055 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F SF susceptible form Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible and only very slightly less active than wild type SL9. Martinez-Hackert2006
54495 SL9 1056 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiAvL Y3F, V6I, T8V Y79F, V82I, T84V SF susceptible form Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1057 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V SF susceptible form Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1058 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I SF susceptible form Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1059 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNsVATL T5S T81S SF susceptible form Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1060 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYqTVATL N4Q N80Q SF susceptible form Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1061 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYlTVATL N4L N80L SF susceptible form Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible. Martinez-Hackert2006
54495 SL9 1062 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL aLYNTVATL S1A S77A SF susceptible form Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL was susceptible, indistinguishable from the wild type SL9. Martinez-Hackert2006
54495 SL9 1063 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLaNTVATL Y3A Y79A NSF non-susceptible form Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL elicited no response. Martinez-Hackert2006
54495 SL9 1064 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYaTVATL N4A N80A NSF non-susceptible form Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL elicited no response. Martinez-Hackert2006
54495 SL9 1065 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTaATL V6A V82A DR diminished response Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL has very low activity. Martinez-Hackert2006
54495 SL9 1066 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAaL T8A T84A DR diminished response Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL was less active. Martinez-Hackert2006
54495 SL9 1067 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL aLYNTaAaL S1A, V6A, T8A S77A, V82A, T84A NSF non-susceptible form Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL elicited no response. Martinez-Hackert2006
54495 SL9 1068 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNvVATL T5V T81V NSF non-susceptible form Chromium-release assay, Sequence This synthetic variant when tested in the presence of D3 TCR, Gag-specific CTL elicited no response. Martinez-Hackert2006
74 SL9 1111   B A Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNaiAvL Y3F, T5A, V6I, T8V Y79F, T81A, V82I, T84V SNSF subtype-specific non-susceptible form Chromium-release assay Recombinant vaccinia virus containing this Clade A circulating Ugandan variant was not recognized by a CTL clone from a Clade B-infected patient. McAdam1998
74 SL9 1112   B A Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVATL Y3F Y79F SNSF subtype-specific non-susceptible form Chromium-release assay Recombinant vaccinia virus containing this Clade A circulating Ugandan variant was not recognized by a CTL clone from a Clade B-infected patient. McAdam1998
74 SL9 1113   B D Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiATL V6I V82I SSF subtype-specific susceptible form Chromium-release assay Recombinant vaccinia virus containing this Clade D circulating Ugandan variant was well recognized by a CTL clone from a Clade B-infected patient. A natural variant with the same substitution was found in the same Clade B carrying patient. McAdam1998
53411 SLF 1349       Gag 77 85 p17(77-85) 1018..1044 A2 SLFNTVATL SLyNTVATL F3Y F79Y E escape documented in this paper CD8 T-cell Elispot - IFNy, Sequence, Tetramer binding Positive selection on this epitope resulted in an escape by phylogenetic analysis. The variant peptide was less potent at inducing production of IFN-gamma than the index peptide. Oxenius2004
53411 SLF 1350       Gag 77 85 p17(77-85) 1018..1044 A2 SLFNTVATL SLyNaVATL F3Y, T5A F79Y, T81A E escape documented in this paper CD8 T-cell Elispot - IFNy, Sequence, Tetramer binding Positive selection on this epitope resulted in an escape by phylogenetic analysis. The variant peptide was less potent at inducing production of IFN-gamma than the index peptide. Oxenius2004
101 SL9 1542   B A Gag 77 85 p17(77-85) 1018..1044 A*0202, A2 SLYNTVATL SLfNTVATL Y3F Y79F SF susceptible form Chromium-release assay Two HEPS Kenyan subjects cross-reacted to this B clade epitope and one of them elicited a stronger reaction to the A clade form, SLfNTVATL Rowland-Jones1998
83 SL9 1555   B, D A Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F OV observed variant Chromium-release assay 5/6 Kenyan HEPS subjects recognized this clade B epitope which differed from the clade A variant, SLfNTVATL. RowlandJones1998b
82 SL9 1622   B B Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V SF susceptible form Chromium-release assay This naturally occurring, strain MANC variant, was recognized by a Patient LWF CTL clone. Sipsas1997
82 SL9 1623   B B Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V SF susceptible form Chromium-release assay This naturally occurring, strain NY5CG variant, was recognized by a Patient LWF CTL clone. Sipsas1997
55395 Gag 77 1658       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subjects Pt15, Pt18 carried this variant epitope, but cross-recognized the challenge HXB2 sequence SLYNTVATL. Subject Pt30 who carried the challenge epitope too did not recognize that HXB2 sequence. Thorn2007
55395 Gag 77 1660       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subject P43 carried this variant epitope, but cross-recognized the challenge HXB2 sequence SLYNTVATL. Subject Pt21 who also carried the variant epitope did not recognize HXB2 sequence. Thorn2007
55395 Gag 77 1661       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVATi L9I L85I OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subject Pt23 carried this variant epitope, and recognized the challenge HXB2 sequence SLYNTVATL. Thorn2007
55395 Gag 77 1662       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATi Y3F, L9I Y79F, L85I OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subject Pt41 carried this variant epitope, and recognized the challenge HXB2 sequence SLYNTVATL. Thorn2007
55395 Gag 77 1663       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLnNaiAvL Y3N, T5A, V6I, T8V Y79N, T81A, V82I, T84V OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subject Pt17 carried this variant epitope, and did not recognize the challenge HXB2 sequence SLYNTVATL. Thorn2007
55700 SL9 1830       Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLYNTiATL V6I V82I SF susceptible form Sequence, TCR binding This natural variant was found in 1/12 proviruses of patient 868 and bound isolated wild type TCR with high affinity. High-affinity, mutated a11b6 TCR also bound this variant. Varela-Rohena2008
55700 SL9 1831       Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLfNTVATL Y3F Y79F SF susceptible form Intracellular cytokine staining, Sequence, TCR binding This naturally occurring variant was recognized by a CTL line from patient 868. Wild type 868 TCR also bound this variant. Binding to high-affinity TCR (a11b6) increased the magnitude of cytokine response. Varela-Rohena2008
55700 SL9 1832       Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V SF susceptible form Intracellular cytokine staining, Sequence, TCR binding This naturally occurring variant was recognized by a CTL line from patient 868. Wild type 868 TCR also bound this variant. Binding to high-affinity TCR (a11b6) increased the magnitude of cytokine response, though this binding was the weakest of all variants tested. Varela-Rohena2008
55700 SL9 1833       Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLfNTiAvL Y3F, V6I, T8V Y79F, V82I, T84V SF susceptible form Intracellular cytokine staining, Sequence, TCR binding This naturally occurring variant was recognized by a CTL line from patient 868 and found in 11/12 sequenced proviruses. Wild type 868 TCR also bound this variant. Binding to high-affinity TCR (a11b6) increased the magnitude of cytokine response. Varela-Rohena2008
55700 SL9 1834       Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLhNTVATL Y3H Y79H E, TCR escape documented in this paper, TCR related mutation Sequence, Surface Plasmon Resonance, TCR binding This unusual SL9 escape variant was recognized poorly by patient 868 CTL, suggesting that viruses with this mutation would escape wild type TCR recognition. High affinity a11b6 TCR, however, did bind this variant well enough by surface plasmon resonance to predict recognition. Varela-Rohena2008
52791 SL9 1856 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F E, SF, TCR escape documented in this paper, susceptible form, TCR related mutation Chromium-release assay, Relative replication capacity assay, Sequence CTL Clone 161JxA14 recognizes this variant but Clone 18030D23 from a different subject does not. Both clones recognize SL9 index sequence similarly. Yang2003
52791 SL9 1857 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiATL V6I V82I E escape documented in this paper Chromium-release assay, Sequence After 2 weeks of selective pressure by culturing with 1 of 4 SL9-specific clones i.e. 161JxA14, this variant arose and was not recognized. Yang2003
52791 SL9 1858 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V E, NSF, SF, TCR escape documented in this paper, non-susceptible form, susceptible form, TCR related mutation Chromium-release assay, Relative replication capacity assay, Sequence CTL Clone 18030D23 recognizes this variant but Clone 161JxA14 from a different subject does not. Both clones recognize SL9 Clade B index sequence similarly. Since the clones are from different HIV-1 infected subjects, with different TCR sequences, TCR is seen to contribute to escape differentially in this instance. Yang2003
52791 SL9 1859 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I E, NSF, SF, TCR escape documented in this paper, non-susceptible form, susceptible form, TCR related mutation Chromium-release assay, Relative replication capacity assay, Sequence CTL Clone 18030D23 recognizes this variant but Clone 161JxA14 from a different subject does not. Both clones recognize SL9 index sequence similarly. Since the clones are from different HIV-1 infected subjects, with different TCR sequences, TCR is seen to contribute to escape differentially in this instance. Yang2003
52791 SL9 1860 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNlVAvL T5L, T8V T81L, T84V E, NSF, TCR escape documented in this paper, non-susceptible form, TCR related mutation Chromium-release assay, Relative replication capacity assay, Sequence CTL Clones 18030D23 and 161JxA14 from different subjects do not recognize this variant. Both clones recognize SL9 index sequence similarly. Since the clones are from different HIV-1 infected subjects, with different TCR sequences, TCR is seen to contribute to escape differentially in this instance. Yang2003
52791 SL9 1861 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAaL T8A T84A OV observed variant Chromium-release assay, Sequence This minority epitope variant was seen after 2 weeks of selection by SL9-specific clone 18030D23. Yang2003
53157   1878       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiATL V6I V82I E, P, SF escape documented in this paper, processing, susceptible form Chromium-release assay Index epitope SL9 and this variant escaped from killing by Gag-epitope-specific CTL clonal lines when presented as endogenously expressed sequences on transformed cells, but were recognized when exogenously loaded as synthetic peptide. A processing or epitope presentation mutation is assumed. Yokomaku2004
53157   1881       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SvYNTVATL L2V L78V E, P, SF escape documented in this paper, processing, susceptible form Chromium-release assay This variant escaped from killing by Gag-epitope-specific CTL clonal lines when presented as an endogenously expressed sequence on transformed cells, but was recognized when exogenously loaded as synthetic peptide. A processing or epitope presentation mutation is assumed. Yokomaku2004
53157   1882       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNlVATL T5L T81L E, P, SF escape documented in this paper, processing, susceptible form Chromium-release assay This variant escaped from killing by Gag-epitope-specific CTL clonal lines when presented as an endogenously expressed sequence on transformed cells, but was recognized when exogenously loaded as synthetic peptide. A processing or epitope presentation mutation is assumed. Yokomaku2004
53157   1883       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVAvL Y3F, T8V Y79F, T84V E, P, SF escape documented in this paper, processing, susceptible form Chromium-release assay This variant escaped from killing by Gag-epitope-specific CTL clonal lines when presented as an endogenously expressed sequence on transformed cells, but was recognized when exogenously loaded as synthetic peptide. A processing or epitope presentation mutation is assumed. Yokomaku2004
54495 SL9 2224 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNlVAvL T5L, T8V T81L, T84V E, TCR escape documented in this paper, TCR related mutation Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL abolished CTL recognition, but was still able to bind HLA-A2. Martinez-Hackert2006
54495 SL9 2248 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNlVAvL T5L, T8V T81L, T84V E, TCR escape documented in this paper, TCR related mutation Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL abolished CTL recognition, but was still able to bind HLA-A2. Martinez-Hackert2006
54495 SL9 2250 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNaVATL T5A T81A E, TCR escape documented in this paper, TCR related mutation Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL abolished CTL recognition, but was still able to bind HLA-A2. Martinez-Hackert2006
54495 SL9 2251 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNaiATL T5A, V6I T81A, V82I E, TCR escape documented in this paper, TCR related mutation Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL abolished CTL recognition, but was still able to bind HLA-A2. Martinez-Hackert2006
54495 SL9 2252 B     Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNlVAvL T5L, T8V T81L, T84V E, TCR escape documented in this paper, TCR related mutation Chromium-release assay, Sequence This natural variant when tested in the presence of D3 TCR, Gag-specific CTL abolished CTL recognition, but was still able to bind HLA-A2. Martinez-Hackert2006
54497 SL9 2256       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V DR, SF diminished response, susceptible form   This variant was recognized by both SL9-CTLs and by the T/A-variant CTLs from two patients, but to somewhat lesser extent than the wt epitope in one of the patients. Kan-Mitchell2006
55395 Gag 77 2264       Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SvYNTVATL L2V L78V OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subject Pt33 carried this variant, and did not recognize the challenge HXB2 SLYNTVATL. Thorn2007
55700 SL9 2279       Gag 77 85 p17(77-85) 1018..1044 A*02 SLYNTVATL SLYaaaAaL N4A, T5A, V6A, T8A N80A, T81A, V82A, T84A SF susceptible form TCR binding A patient 868 CTL line showed some recognition of this multiply substituted peptide. Varela-Rohena2008
57381 SL9 2340 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V LE literature escape CD8 T-cell Elispot - IFNy, Chromium-release assay SL9 variant V82I/T84V, SLYNTiAvL, was recognized by different TCR mutants with differing functional avidities. Bennett2010
57381 SL9 2341 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVATL Y3F Y79F LE literature escape CD8 T-cell Elispot - IFNy, Chromium-release assay SL9 variant Y79F, SLfNTVATL, was recognized by different TCR mutants with differing functional avidities. Bennett2010
57381 SL9 2342 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiATL V6I V82I LE literature escape CD8 T-cell Elispot - IFNy, Chromium-release assay SL9 variant V82I, SLYNTiATL, was recognized by different TCR mutants with differing functional avidities. Bennett2010
57719   2617       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVATL Y3F Y79F SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant SLfNTVATL was seen in patient I09. Vollbrecht2010
57719   2618       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiATL V6I V82I SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant SLYNTiAL was seen in patients I11, I07 and C06. Vollbrecht2010
57719   2619       Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant SLfNTiATL was seen in patients I07. Vollbrecht2010
57959 SL9 2690 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVVTL SLYNTVaTL V7A V83A SF susceptible form CD8 T-cell Elispot - IFNy SLYNTVVTL underwent adaptation to neo-epitope SLYNTVaTL. 4 subjects had higher EliSpot responses to the neo-epitope than to the non-adapted form. Keane2012
58010 SL9 2705 B B B Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTVAvL T8V T84V A, P HLA association, processing   A2-SL9 has known HLA-associated mutants (T8V, Y3F, V6I, V6I/T8V, Y3F/V6I). All 5 mutants displayed severely reduced half-lives. Lazaro2011
58010 SL9 2706 B B B Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTVATL Y3F Y79F A, P HLA association, processing   A2-SL9 has known HLA-associated mutants (T8V, Y3F, V6I, V6I/T8V, Y3F/V6I). All 5 mutants displayed severely reduced half-lives. Lazaro2011
58010 SL9 2707 B B B Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiATL V6I V82I A, P HLA association, processing   A2-SL9 has known HLA-associated mutants (T8V, Y3F, V6I, V6I/T8V, Y3F/V6I). All 5 mutants displayed severely reduced half-lives. Lazaro2011
58010 SL9 2708 B B B Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V A, P HLA association, processing   A2-SL9 has known HLA-associated mutants (T8V, Y3F, V6I, V6I/T8V, Y3F/V6I). All 5 mutants displayed severely reduced half-lives. Lazaro2011
58010 SL9 2709 B B B Gag 77 85 p17(77-85) 1018..1044 A2 SLYNTVATL SLfNTiATL Y3F, V6I Y79F, V82I A, P HLA association, processing   A2-SL9 has known HLA-associated mutants (T8V, Y3F, V6I, V6I/T8V, Y3F/V6I). All 5 mutants displayed severely reduced half-lives. Lazaro2011
57182 SL9 2963 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTVAvL T9V T85V DHB, E, LE, SF diminished HLA binding or increased off-rate, escape documented in this paper, literature escape, susceptible form CD8 T-cell Elispot - IFNy, HLA binding, Sequence CTL selection at TCR contact residues is predicted to drive SL9 (SLYNTVATL) to SLYNTVAvL, reversion to SL9 is predicted to result from selection for optimal viral growth. This variant did not bind HLA-A*02 in vitro; and could not elicit response in 2/3 chronically-infected, untreated patients, but showed a complete EliSpot response in the other patient when compared to that elicited by wt peptide SL9. The authors designate all T84V-mutation containing peptides to be escapes. Tenzer2009
57182 SL9 2965 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 {r}SLYNTVATL {k}SLfNTVAvL -1K, Y4F, T9V -77K, Y80F, T85V LE literature escape Sequence CTL selection at TCR contact residues is predicted to drive {k}SLYNTVAvL (SL9-V) to {k}SLfNTVAvL (SL9-KFV); reversion to SL9-V is predicted to result from selection for optimal viral growth. Tenzer2009
57182 SL9 2966 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 {r}SLYNTVATL {k}SLfNTiAvL -1K, Y4F, V7I, T9V -77K, Y80F, V83I, T85V LE literature escape Sequence CTL selection at TCR contact residues is predicted to drive {k}SLfNTVAvL (SL9-KFV) or {k}SLfNTiATL(SL9-KFI) or {r}SLFNTiAvL(SL9-IV) to {k}SLfNTiAvL (SL9-KFIV), reversion to SL9-KFV is predicted to result from selection for optimal viral growth. Tenzer2009
57182 SL9 2967 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 {r}SLYNTVATL {k}SLYNTVATL -1K -77K LE literature escape Sequence Epitope rSLYNTVATL is seen to vary to {k}SLYNTVATL (SL9-K). Tenzer2009
57182 SL9 2968 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLfNTVATL Y3F Y79F E, LE, SF escape documented in this paper, literature escape, susceptible form CD8 T-cell Elispot - IFNy, HLA binding, Longitudinal study CTL selection at TCR contact residues is predicted to drive SL9 (SLYNTVATL) to SLfNTVATL (SL9-F); reversion to SL9 is predicted to result from selection for optimal viral growth. This variant showed a slight increase in EliSpot responses in 2/3 chronically-infected, untreated patients when compared to SL9. Tenzer2009
57182 SL9 2969 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 {r}SLYNTVATL {k}SLfNTiATL -1K, Y4F, V7I -77K, Y80F, V83I LE literature escape Sequence CTL selection at TCR contact residues is predicted to drive SL9-KF {k}SLfNTVATL to {k}SLfNTiATL (SL9-KFI), reversion to SL9-KF is predicted to result from selection for optimal viral growth. Tenzer2009
57182 SL9 2970 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 {r}SLYNTVATL {k}SLfNTVATL -1K, Y4F -77K, Y80F LE literature escape Sequence CTL selection at TCR contact residues is predicted to drive epitope {k}SLYNTVATL (SL9) to variant, {k}SLfNTVATL (SL9-KF). Tenzer2009
57182 SL9 2971 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiATL V6I V82I DHB, DR, E, LE, SF diminished HLA binding or increased off-rate, diminished response, escape documented in this paper, literature escape, susceptible form CD8 T-cell Elispot - IFNy, HLA binding, Sequence CTL selection at TCR contact residues is predicted to drive SL9 (SLYNTVATL) to SLYNTiATL (SL9-I); reversion to SL9 is predicted to result from selection for optimal viral growth. This variant shows a loss of binding to HLA-A*02 in vitro; and is unable to generate a CTL response in 1 chronically-infected, untreated patient, with slight decrease in EliSpot in 2 others as compared to wt peptide SL9. The authors refer to all V82I mutation-containing peptides as escapes. Tenzer2009
57182 SL9 2972 B B B Gag 77 85 p17(77-85) 1018..1044 A*0201 SLYNTVATL SLYNTiAvL V6I, T8V V82I, T84V DHB, E, LE, SF diminished HLA binding or increased off-rate, escape documented in this paper, literature escape, susceptible form CD8 T-cell Elispot - IFNy, HLA binding, Sequence CTL selection at TCR contact residues is predicted to drive SL9-I (SLYNTiATL) to SLYNTiAvL (SL9-IV); reversion to SL9-I is predicted to result from selection for optimal viral growth. This variant could not bind HLA-A*02 in vitro; and did not elicit EliSpot responses in 2/3 chronically-infected, untreated patients, but it showed an increased CTL response in the third patient as compared to WT SL9. The authors designate all V82I and T84V mutation-containing peptides as escapes. Tenzer2009
57298 SY10 2988 B B B Gag 77 86 p17(77-86) 1018..1047 A*02 SLYNTVATLY SLYNTVAvLY T8V T84V DHB, E, SF diminished HLA binding or increased off-rate, escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Variant SLYNTVAvLY could not bind HLA-A*02 in vivo; but did elicit ex-vivo EliSpot responses in at least 1 of 3 chronically-infected, untreated patients. The authors refer to all T84V mutation-containing peptides as escapes. Tenzer2009
57298 SY10 2989 B B B Gag 77 86 p17(77-86) 1018..1047 A*02 SLYNTVATLY SLYNTiATLY V6I V82I DHB, E, SF diminished HLA binding or increased off-rate, escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Variant SLYNTiATLY could not bind HLA-A*02 in vivo; but did elicit ex-vivo EliSpot responses in at least 2 of 3 chronically-infected, untreated patients. The authors refer to all V82I mutation-containing peptides as escapes. Tenzer2009
57298 SY10 2990 B B B Gag 77 86 p17(77-86) 1018..1047 A*02 SLYNTVATLY SLYNTiAvLY V6I, T8V V82I, T84V DHB, E, SF diminished HLA binding or increased off-rate, escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Variant SLYNTiAvLY could not bind HLA-A*02 in vivo; but did elicit ex-vivo EliSpot responses in at least 1 of 3 chronically-infected, untreated patients. The authors refer to all V82I and T84V mutation-containing peptides as escapes. Tenzer2009
57298 SY10 2991 B B B Gag 77 86 p17(77-86) 1018..1047 A*02 SLYNTVATLY SLfNTVATLY Y3F Y79F DHB, E, SF diminished HLA binding or increased off-rate, escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Variant SLfNTVATLY could not bind HLA-A*02 in vitro; but did elicit ex-vivo EliSpot responses in at least 2 of 3 chronically-infected, untreated patients. The authors refer to all Y79F mutation-containing peptides as escapes. Tenzer2009
57298 SY10 2992 B B B Gag 77 86 p17(77-86) 1018..1047 A*02 SLYNTVATLY SLfNTiAvLY Y3F, V6I, T8V Y79F, V82I, T84V DHB, E, SF diminished HLA binding or increased off-rate, escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Variant SLfNTiAvLY could not bind HLA-A*02 in vitro; but did elicit ex-vivo EliSpot responses in at least 2 of 3 chronically-infected, untreated patients. The authors refer to all Y79F, V82I and T84V mutation-containing peptides as escapes. Tenzer2009
57298 SY10 2993 B B B Gag 77 86 p17(77-86) 1018..1047 A*02 SLYNTVATLY SLfNTVAvLY Y3F, T8V Y79F, T84V DHB, E, SF diminished HLA binding or increased off-rate, escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Variant SLfNTVAvLY could not bind HLA-A*02 in vitro; but did elicit ex-vivo EliSpot responses in at least 1 of 3 chronically-infected, untreated patients. The authors refer to all Y79F mutation-containing peptides as escapes. Tenzer2009
57298 SY10 2994 B B B Gag 77 86 p17(77-86) 1018..1047 A*02 SLYNTVATLY SLfNTiATLY Y3F, V6I Y79F, V82I DHB, E, SF diminished HLA binding or increased off-rate, escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Variant SLfNTiATLY could not bind HLA-A*02 in vitro; but did elicit ex-vivo EliSpot responses in at least 2 of 3 chronically-infected, untreated patients. The authors refer to all Y79F mutation-containing peptides as escapes. Tenzer2009
53612   64 A, D     Gag 77 91 p17(77-91) 1018..1062 A*0201, A*3002 SLYNTVATLYCVHQR SLfNTVATLYCVHQR Y3F Y79F SF susceptible form CD8 T-cell Elispot - IFNy The sequence contains a known A2 epitope and a known A*3002 epitope, and the subjects recognizing it each carry an HLA with a previously-defined restriction. The viral sequence isolated from the subjects was slFntvatlycvhqr, and was reactive. Barugahare2005
55939 LY9(p17) 1906 B B B Gag 78 86 p17(78-86) 1021..1047   LFNTVATLY LyNTVATLY F2Y F79Y OV observed variant CD8 T-cell Elispot - IFNy, Sequence This Asian B Clade optimal epitope differs from the consensus B at one position. It is predicted to be HLA-A29 restricted and possibly HLA-B44 restricted. Experimentally, B clade consensus peptide was used to challenge CTL response in subjects commonly carrying the Asian B-type epitope. Zhai2008
55634   14 CRF02_AG, CRF01_AE AG AE Gag 79 90 p17(79-90) 1024..1059   YNIVATLWCVHQ YNtVATLWCVHQ I3T I81T SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy 1 subject responded to peptide YNIVATLWCVHQ from subtype CRF02_AG and to peptide YNtVATLWCVHQ from subtype CRF01_AE. Aidoo2008
55367 Gag 80 1664       Gag 80 88 p17(80-88) 1027..1053 A2 NTVATLYCV NaiAvLYCV T2A, V3I, T5V T81A, V82I, T84V OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subjects Pt15, Pt16, Pt18, Pt30, Pt33 and Pt35 carried this HXB2 epitope. All of the above were unable to recognize it however, except for Pt15 who did recognize the HXB2 sequence. Only Pt17 carried the variant NaiAvLYCV and was unable to cross-recognize the challenge HXB2 sequence. Thorn2007
55367 Gag 80 1665       Gag 80 88 p17(80-88) 1027..1053 A2 NTVATLYCV NTVAvLYCV T5V T84V OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subjects Pt21 and Pt43 carried this variant and were unable to recognize the challenge HXB2 form, NTVATLYCV. Thorn2007
55367 Gag 80 1666       Gag 80 88 p17(80-88) 1027..1053 A2 NTVATLYCV NTVATiYCV L6I L85I OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subjects Pt23 and Pt41 carried this variant and were unable to recognize the challenge HXB2 form, NTVATLYCV. Thorn2007
55367 Gag 80 1667       Gag 80 88 p17(80-88) 1027..1053 A2 NTVATLYCV NTVATLYCV     OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subject Pt21 carried this variant and was unable to recognize the challenge HXB2 form, NTVATLYCV. Thorn2007
57304 IR10 2964 B B B Gag 82 91 p17(82-91) 1033..1062 A*11 IAVLYCVHQR IvVLYCVHQR A2V A83V OV observed variant CD8 T-cell Elispot - IFNy, HLA binding Variant A11-VR10, IvVLYCVHQR, may also be present and is restricted by the same HLA, A*11. Tenzer2009
57708   2600       Gag 82 92 p17(82-92) 1033..1065 A*11 VATLYCVHQRI VvTLYCVHQRI A2V A83V SF susceptible form CD8 T-cell Elispot - IFNy Gag variant at anchor position 2, VvTLYCVHQRI, also elicited CTL response but from week 24 after TI began in Patient 313. Schweighardt2010
55635   15 CRF02_AG, CRF01_AE AG AE Gag 83 94 p17(83-94) 1036..1071   ATLWCVHQRIDI ATLWCVHQRIev D11E, I12V D93E, I94V SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy 1 subject responded to peptide ATLWCVHQRIDI from subtype CRF02_AG and to peptide ATLWCVHQRIev from subtype CRF01_AE. Aidoo2008
52106   290 B B B Gag 84 91 p17(84-91) 1039..1062 A*1101 TLYCVHQR TLYCVHQk R8K R91K SF susceptible form Chromium-release assay Variant predominantly found in clade B. There was some CTL activity in PBMC from clade B patients stimulated with this epitope variant. Fukada2002
52106   291 B B CRF01_AE Gag 84 91 p17(84-91) 1039..1062 A*1101 TLYCVHQR TLwCVHQR Y3W Y86W OV observed variant   Variant predominantly found in clade E. Fukada2002
52106   292 B B D Gag 84 91 p17(84-91) 1039..1062 A*1101 TLYCVHQR TLYCVHeR Q7E Q90E OV observed variant   Variant predominantly found in clade D. Fukada2002
107   412       Gag 84 91 p17(84-91) 1039..1062 A11 TLYCVHQR TLYCVHQk R8K R91K SF susceptible form Chromium-release assay Variant found in patient. It was recognized by patient CTLs and induced target specific lysis. Harrer1998
107   413       Gag 84 91 p17(84-91) 1039..1062 A11 TLYCVHQR TLYCVHQq R8Q R91Q DR diminished response Chromium-release assay Variant found in patient. It was recognized by patient CTLs but less than the R/K variant, and only induced target specific lysis at high concentrations. This mutation did not abrogate virus replication. Harrer1998
107   414       Gag 84 91 p17(84-91) 1039..1062 A11 TLYCVHQR TLYCVHeR Q7E Q90E E escape documented in this paper Chromium-release assay Variant found in patient. It was not able to induce target specific lysis. This mutation did not abrogate virus replication. Harrer1998
54579 EL9 637 B     Gag 93 101 p17(93-101) 1066..1092 B*08 EVKDTKEAL dVKDTKEAL E1D E93D DR diminished response CD8 T-cell Elispot - IFNy Variant found in one patient at week 63. A minor response to this variant, but the variant was eliminated by CTLs. R91G upstream mutation affects processing. Karlsson2007
54579 EL9 638 B     Gag 93 101 p17(93-101) 1066..1092 B*08 EVKDTKEAL EiKDTKEAL V2I V94I IE inferred escape CD8 T-cell Elispot - IFNy Author tabulates this variant detected in 9/14 clones at week 39 in patient OP428 as viral escape. No CTL response detected. Karlsson2007
54579 EL9 639 B     Gag 93 101 p17(93-101) 1066..1092 B*08 EVKDTKEAL kVKDTKEAL E1K E93K IE inferred escape CD8 T-cell Elispot - IFNy Author tabulates this variant detected in 1/11 clones at week 139 in patient OP428 as viral escape. No CTL response detected. Karlsson2007
54579 EL9 640 B     Gag 93 101 p17(93-101) 1066..1092 B*08 EVKDTKEAL EVKDTKgAL E7G E99G IE inferred escape CD8 T-cell Elispot - IFNy Author tabulates this variant detected in 1/16 clones at week 15 in patient OP428 as viral escape. No CTL response detected. Karlsson2007
55237   795 B, CRF01_AE   B Gag 93 101 p17(93-101) 1066..1092 B8 EIKDTKEAL EvKDTKEAL I2V I94V OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in B1. Kozaczynska2007
55237   797 B, CRF01_AE   B Gag 93 101 p17(93-101) 1066..1092 B8 EIKDTKEAL dvKDTKEAL E1D, I2V E93D, I94V OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in B2 and it did not change over time. Kozaczynska2007
55237   798 B, CRF01_AE   CRF01_AE Gag 93 101 p17(93-101) 1066..1092 B8 EIKDTKEAL EIlDTKEAL K3L K95L OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in CRF01_AE and it did not change over time. Kozaczynska2007
53822   1308 B     Gag 93 101 p17(93-101) 1066..1092 B*0801 EVKDTKEAL dVKgTKEAL E1D, D4G E93D, D96G E escape documented in this paper CD8 T-cell Elispot - IFNy, Sequence This variant was found in Donor2 but not transmitted to Recipient2. The variant was not recognized by CTL. Both donor and recipient carried the restricting HLA-B*0801 allele Milicic2005
53822   1309 B     Gag 93 101 p17(93-101) 1066..1092 B*0801 EVKDTKEAL dVKDTKEAL E1D E93D E, SF escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, Sequence This variant was found in Donor2 and Recipient2 both of whom were restricting HLA-B*0801 carriers. The variant was not recognized by CTL in Donor2, but was recognized in Recipient2 from whom it was driven out de novo in time. Milicic2005
55237   2258 B, CRF01_AE   B Gag 93 101 p17(93-101) 1066..1092 B8 EIKDTKEAL dIKDTKEAL E1D E93D R reversion Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This reversion variant developed in B1 to include 83% of the viruses within 4 years. Kozaczynska2007
57704   2598       Gag 93 101 p17(93-101) 1066..1092 B*08 EIKDTKEAL EvKDTKEAL I2V I94V SF susceptible form CD8 T-cell Elispot - IFNy Gag variant EvKDTKEAL was recognized by CTL 48 weeks into TI, in Patient 311. Schweighardt2010
57704   2599       Gag 93 101 p17(93-101) 1066..1092 B*08 EIKDTKEAL dvKDTKEAL E1D, I2V E93D, I94V SF susceptible form CD8 T-cell Elispot - IFNy Gag variant dvKDTKEAL was recognized by CTL 48 weeks into TI, in Patient 311. Schweighardt2010
53223 Gag AQ9 507 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTGNgSQ S7G S125G E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 508 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ eADTGNSSQ A1E A119E E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 509 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTkNSSQ G5K G123K E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 510 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTrNSSQ G5R G123R E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 511 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ eADTGkSSQ A1E, N6K A119E, N124K E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 512 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTGNSSk Q9K Q127K E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 513 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTGsSSQ N6S N124S E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 514 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ tADTGNSns A1T, S8N, Q9S A119T, S126N, Q127S E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 515 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTGNnnQ S7N, S8N S125N, S126N E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 516 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ A-DTGNSSQ A2- A120- OV observed variant   1/15 clones at time point 35. Jones2004
53223 Gag AQ9 517 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AAgTGNSSQ D3G D121G OV observed variant   1/15 clones at time point 55. Jones2004
53223 Gag AQ9 518 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTeNSSQ G5E G123E OV observed variant   2/15 clones at time point 55 and 1/15 clones at time point 65. Jones2004
53223 Gag AQ9 2285 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTGN-S-(ss) S7-, Q9-, -(9.1)S, -(9.2)S S125-, Q127-, -(127.1)S, -(127.2)S E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 2287 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ tADTGN-Sn(s) A1T, S7-, Q9N, -(9.1)S A119T, S125-, Q127N, -(127.1)S E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
53223 Gag AQ9 2288 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTGNnS(ns)Q S7N, -(8.1)N, -(8.2)S S125N, -(126.1)N, -(126.2)S OV observed variant   1/15 clones at time point 556. Jones2004
53223 Gag AQ9 2299 B     Gag 119 127 p17(119-127) 1144..1170   AADTGNSSQ AADTGN-S(ss)Q S7-, -(8.1)S, -(8.2)S S125-, -(126.1)S, -(126.2)S E escape documented in this paper   Variant dramatically reduced CTL recognition. Jones2004
56010 NY9(p17) 1907 B B B Gag 124 132 p17(124-132) 1159..1185   NSSQVSQNY NSSkVSQNY Q4K Q127K OV observed variant CD8 T-cell Elispot - IFNy, Sequence This Asian B Clade optimal epitope differs from the consensus B at one position. It is predicted to be HLA-B35 restricted. Experimentally, B clade consensus peptide was used to challenge CTL response in subjects commonly carrying the Asian B-type epitope. Zhai2008
53224 Gag NP10 519 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NgSQVSQNYP S2G S125G DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 520 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NSSQaSQNYP V5A V128A DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 521 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP sSSQVSQNYP N1S N124S DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 522 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NSSQdSQNYP V5D V128D DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 523 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NSSQgSQNYP V5G V128G DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 524 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP kSSQVSQNYP N1K N124K DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 525 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NSSkVSQNYP Q4K Q127K DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 526 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NmnQVSQNYP S2M, S3N S125M, S126N DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 2289 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NSS(s)QVSQNYP -(3.1)S -(126.1)S DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 2290 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NS(n)SQVSQNYP -(2.1)N -(125.1)N DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
53224 Gag NP10 2291 B     Gag 124 133 p17(124)-p24(1) 1159..1188   NSSQVSQNYP NnS(ns)QVSQNYP S2N, -(3.1)N, -(3.2)S S125N, -(126.1)N, -(126.2)S DR diminished response   Confirmed some degree of escape by diminishing CTL response. Jones2004
54628 GAG-18 2269 B B C Gag 126 143 p17(126)-p24(11) 1165..1218   SQVSQNYPIVQNLQGQMV -kVSQNYPIVQNLQGQMV S1-, Q2K S126-, Q127K SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence This Clade C consensus synthetic peptide variant from an immunodominant region, differs from the immunodominant Clade B consensus at 2 amino acids (11.1%) and both were recognized by subtype-B-infected subjects. Zhao2007
53592 Gag 7.3 55   B CRF02_AG Gag 129 139 p17(129)-p24(7) 1174..1206   SQNYPIVQNIQ SQNYPIVQNaQ I10A I138A SNSF subtype-specific non-susceptible form Intracellular cytokine staining, T-cell Elispot The response elicited to the B clade epitope SQNYPIVQNIQ does not cross-react with the CRF02 form SQNYPIVQNaQ Amara2005a
58386 Peptide 32 2915 C C D Gag 129 143 p17(129)-p24(11) 1174..1218   xxxSQNYPIVQNLQG sqvSQNYPIVQNLQG x1S, x2Q, x3V x129S, x130Q, x131V SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-D peptide 32, sqvSQNYPIVQNLQG, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58386 Peptide 32 2916 C C A Gag 129 143 p17(129)-p24(11) 1174..1218   xxSQNYPIVQNLQGM kvSQNYalkhrayel x1K, Q10H, N11R, L12A, Q13Y, G14E, M15L, x2V, P7A, I8L, V9K x129K, Q138H, N139R, L140A, Q141Y, G142E, M143L, x130V, P135A, I136L, V137K SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-A peptide 32, kvSQNYalkhrayel, did not elicit a response from South African subjects carrying clade-C virus. Zembe2011
58174 GI8 2781       Gag 140 147 p24(8-15) 1207..1230 B*4801 GQMVHQAI GQMVHQpI A7P A146P A, E HLA association, escape documented in this paper Intracellular cytokine staining Variant GQMVHQpI, A146P, was shown to be an escape and was strongly associated with HLA allele B*4801 among HIV-1 infected Japanese. Naruto2011Kawashima2009
55234   799 B, CRF01_AE   B Gag 140 153 p24(8-21) 1207..1248 A3, Cw3 GQMVHQAISPRTLN GQMVHQpISPRTLN A7P A146P OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in B1 and B2, and it did not change over time. Kozaczynska2007
55234   800 B, CRF01_AE   CRF01_AE Gag 140 153 p24(8-21) 1207..1248 A3, Cw3 GQMVHQAISPRTLN GQMVHQpvSPRTLN A7P, I8V A146P, I147V OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in CRF01_AE and it did not change over time. Kozaczynska2007
53613   65 A, D     Gag 141 155 p24(9-23) 1210..1254   QMVHQSLSPRTLNAW QMtHQnLSPRTLNAW V3T, S6N V143T, S146N OV observed variant CD8 T-cell Elispot - IFNy The sequence contains a known B7/B8 epitope, but the subjects recognizing it are B7- and B8-negative. The viral sequences isolated from the subjects were qmThqNlsprtlnaw and qmvhqAlsprtlnaw, and the index peptide was recognized. Barugahare2005
53613   66 A, D     Gag 141 155 p24(9-23) 1210..1254   QMVHQSLSPRTLNAW QMVHQaLSPRTLNAW S6A S146A OV observed variant CD8 T-cell Elispot - IFNy The sequence contains a known B7/B8 epitope, but the subjects recognizing it are B7- and B8-negative. The viral sequences isolated from the subjects were qmThqNlsprtlnaw and qmvhqAlsprtlnaw, and the index peptide was recognized. Barugahare2005
55639   16 A, CRF02_AG AG A Gag 142 155 p24(10-23) 1213..1254   MVHQSMSPRTLNAW MVHQplSPRTLNAW S5P, M6L S146P, M147L SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy 2 subjects responded to peptide MVHQSMSPRTLNAW from subtype CRF02_AG, and 1 of the 2 responded to peptide MVHQplSPRTLNAW from subtype A. Aidoo2008
55992 HL9(p24) 1908 B B B Gag 144 152 p24(12-20) 1219..1245   HQPISPRTL HQaISPRTL P3A P146A OV observed variant CD8 T-cell Elispot - IFNy, Sequence Experimentally, B clade consensus peptide was used to challenge CTL response in subjects commonly carrying the Asian B-type epitope. This Asian B Clade optimal epitope differs from the consensus B at one position. It is predicted to be HLA-B15 restricted. Zhai2008
54145 QW11 955 B     Gag 145 155 p24(13-23) 1222..1254 A*2501 QAISPRTLNAW QAlSPRTLNAW I3L I147L DR diminished response CD8 T-cell Elispot - IFNy Amino acid site in the third position potentially experienced positive selection. Wt form of the epitope was 2.4 times better recognized than the variant. Liu2006
58160 QW11 2747 B B B Gag 145 155 p24(13-23) 1222..1254 A*2501 QAISPRTLNAW QAlSPRTLNAW I3L I147L SF susceptible form CD8 T-cell Elispot - IFNy, Longitudinal study Major variant QAlSPRTLNAW replaced the wild type sequence by 800 days post-infection. It did not abrogate EliSpot response to the epitope. Liu2011a
58812 ISW9 3172 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 {A}ISPRTLNAW {s}lSPRTLNAW I1L, A-1S I146L, A145S OV observed variant Sequence Flanking and epitope mutations, {s}lSPRTLNAW{V}, were seen for ISW9 by 13 weeks post-infection in patient 1 (P1) who carried HLA alleles A*0101, A*0301, B*2705, B*5701. Norstrom2012
58812 ISW9 3173 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 {A}ISPRTLNAW {p}lSPRTLNAW I1L, A-1P I146L, A145P OV observed variant Sequence Flanking and epitope mutations, {p}lSPRTLNAW{V}, were seen for ISW9 by 104 weeks post-infection in patient 1 (P1) who carried HLA alleles A*0101, A*0301, B*2705, B*5701 and at 179 weeks post-infection in patient 3 (P3) who carried HLA alleles A*2402 , A*3201, B*4002, B*5701. Norstrom2012
58812 ISW9 3174 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 ISPRTLNAW lSPRTLNAW I1L I146L OV observed variant Sequence Epitope mutation, A|lSPRTLNAW|V, was seen for ISW9 by 271 weeks post-infection in patient 1 (P1) who carried HLA alleles A*0101, A*0301, B*2705, B*5701; at 45 weeks post-infection in patient 3 (P3) who carried HLA alleles A*2402 , A*3201, B*4002, B*5701; from 144 weeks post-infection in patient 5 (P5) who carried alleles A*0101,A*0101,B*0801,B*5701 and from 17 weeks post-infection in patient 6 (P6) who carried alleles A*0301,A*2402,B*3501,B*5701. Norstrom2012
58812 ISW9 3175 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 {A}ISPRTLNAW {p}ISPRTLNAW A-1P A145P OV observed variant Sequence Flanking mutation, {p}ISPRTLNAW{V}, was seen for ISW9 from 75 weeks post-infection in patient 3 (P3) who carried HLA alleles A*2402 , A*3201, B*4002, B*5701; from 60 weeks post-infection in P4 who carried HLA alleles A*0101,A*0201,B*5101,B*5701; and from 10 weeks post-infection in P6 who carried HLA alleles A*0301,A*2402,B*3501,B*5701. Norstrom2012
58812 ISW9 3176 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 {A}ISPRTLNAW {p}IaPRTLNAW A-1P, S2A A145P, S147A OV observed variant Sequence Flanking and epitope mutations, {p}IaPRTLNAW{V}, were seen for ISW9 by 274 weeks post-infection in P3 who carried HLA alleles A*2402 , A*3201, B*4002, B*5701. Norstrom2012
58812 ISW9 3177 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 {A}ISPRTLNAW {p}ItPRTLNAW A-1P, S2T A145P, S147T OV observed variant Sequence Flanking and epitope mutations, {p}ItPRTLNAW{V}, were seen for ISW9 by 11 weeks post-infection in P4 who carried HLA alleles A*0101,A*0201,B*5101,B*5701. Norstrom2012
58812 ISW9 3178 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 {A}ISPRTLNAW {p}ltPRTLNAW I1L, A-1P, S2T I146L, A145P, S147T OV observed variant Sequence Epitope mutation, {A}ItPRTLNAW{V}, was seen for ISW9 by 11 weeks post-infection in P4 who carried HLA alleles A*0101,A*0201,B*5101,B*5701. Norstrom2012
58812 ISW9 3179 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 ISPRTLNAW ItPRTLNAW S2T S147T OV observed variant Sequence Flanking and epitope mutations, A|ItPRTLNAW|V, were seen for ISW9 by 316 weeks post-infection in P4 who carried HLA alleles A*0101,A*0201,B*5101,B*5701. Norstrom2012
58812 ISW9 3180 B B B Gag 146 155 p24(14-23) 1225..1254 B*5701 ISPRTLNAW IlPRTLNAW S2L S147L OV observed variant Sequence Flanking and epitope mutations including IlPRTLNAW, were seen for ISW9 by 45 weeks post-infection in P3 who carried HLA alleles A*2402,A*3201,B*4002,B*5701. Norstrom2012
57412 IW9 2353 B B B Gag 146 156 p24(14-24) 1225..1257 B*57 AISPRTLNAWV pISPRTLNAWV A1P A146P OV observed variant Sequence One HLA-B*5703 positive patient with low viral load carried this variant from month 6 after enrollment. Durand2010
57412 IW9 2355 B B B Gag 146 156 p24(14-24) 1225..1257 B*57 AISPRTLNAWV plSPRTLNAWV A1P, I2L A146P, I147L OV observed variant Sequence One HLA-B*5703 positive patient with increased viral load carried this variant from month 10 after enrollment onwards. Durand2010
57412 IW9 2356 B B B Gag 146 156 p24(14-24) 1225..1257 B*57 AISPRTLNAWV pISaRTLNAWV A1P, P4A A146P, P149A OV observed variant Sequence One HLA-B*5701 positive patient with increased viral load carried this variant from enrollment onwards. Durand2010
57412 IW9 2357 B B B Gag 146 156 p24(14-24) 1225..1257 B*57 AISPRTLNAWV AlSPRTLNAWV I2L I147L OV observed variant Sequence One HLA-B*5701 positive patient with low viral load carried this variant, AlSPRTLNAWV, at month 28 after enrollment; One HLA-B*5702 positive patient with low viral load carried it at month 13; and one HLA-B*5703 positive patient with increased viral load carried it from 7 months post-enrollment on. Durand2010
53636 IW9 138 C     Gag 147 155 p24(15-23) 1228..1254 B57 ISPRTLNAW lSPRTLNAW I1L I147L OV observed variant CD8 T-cell Elispot - IFNy ISPRTLNAW had a variant lSPRTLNAW in 7/10 B57+ subjects, and 4/9 B57- subjects; 2 other variants were observed, but there was no apparent sequence selection in this epitope. Currier2005
52917 ISW9 181 B, C     Gag 147 155 p24(15-23) 1228..1254 B57 ISPRTLNAW pSPRTLNAW I1P I147P E, P escape documented in this paper, processing CD8 T-cell Elispot - IFNy, Chromium-release assay The A146P mutation flanking the ISW9 epitope, {p}ISPRTLNAW, is positively selected in HLA-B57+ persons and it prevents trimming of the optimal epitope by the endoplasmic reticulum aminopeptidase I. The A146P processing escape mutation does not influence replicative capacity of the virus in vitro and is accumulated over time in the human population. Draenert2004a
53648 ISW9 196       Gag 147 155 p24(15-23) 1228..1254 B57, B*5801 ISPRTLNAW lSPRTLNAW I1L I147L IE inferred escape Sequence ISPRTLNAW was recognized more often in children than in adults, and was the most frequently recognized B57 epitope in children. Longitudinal sequencing of 2 HLA B57-positive children born to HLA B57-negative mothers and HIV-negative fathers showed variants of this epitope: p|lSPRTLNAW, and lSPRTLNAW. In both cases the mother carried A|ISPRTLNAW, confirming that the mutations arose under selective pressure in the children following vertical transmission. Response to the variants was not studied. Feeney2005a
53675   330 B, D     Gag 147 155 p24(15-23) 1228..1254 B58 ISPRTLNAW lSPRTLNAW I1L I147L OV observed variant   Cross-clade T cell responses are frequently induced in individuals infected with different HIV-1 clades. There was an inverse correlation between the height of responses and epitope sequence divergence. For Gag epitopes, the magnitude of the response was directly linked to the homology between HLA anchor residues. Geels2005
54598   342 A, C C A, D Gag 147 155 p24(15-23) 1228..1254 B57, B58 ISPRTLNAW lSPRTLNAW I1L I147L DR diminished response   The wild type epitope sequence was a subtype C peptide, the variant common to subtypes A and D. CTL response in 56 individuals from Tanzania was strongest for subtypes A and D peptides, and much lower for subtype C, due to point mutation and/or frame-of-epitope effect. Geldmacher2007
54576 IW9 641 B     Gag 147 155 p24(15-23) 1228..1254 B*57 ISPRTLNAW lSPRTLNAW I1L I147L OV observed variant   Variant detected at week 106 in one of the patients, but not in association with antigen processing altering mutation A146P. Karlsson2007
54534 IW9 1021 B B A Gag 147 155 p24(15-23) 1228..1254 B57 ISPRTLNAW lSPRTLNAW I1L I147L SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy Cross-recognition of this variant is seen with both C- and A-clades. Anchor residues are at positions 2 and 9; while the A-clade variant contains a change at position 1 to lSPRTLNAW. Malhotra2007
52758   1280 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW lSPRTLNAW I1L I147L OV observed variant Sequence This variant was seen in 6/10 nonprogressors, 11/12 untreated progressors and 3/5 treated progressors. Migueles2003
52758   1281 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW ISaRTLNAW P3A P149A OV observed variant Sequence This variant was seen in 1/5 treated progressors. Migueles2003
52758   1282 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW ISPRTLNAx W9X W155X OV observed variant Sequence This variant was seen in 1/10 nonprogressors. Migueles2003
52758   1283 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW ISPkTLNAW R4K R150K OV observed variant Sequence This variant was seen in 1/10 nonprogressors. Migueles2003
52758   1284 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW IaPRTLNAW S2A S148A OV observed variant Sequence This variant was seen in 1/12 untreated progressors. Migueles2003
52758   1285 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW mSPRTLNAW I1M I147M OV observed variant Sequence This variant was seen in 1/12 untreated progressors. Migueles2003
52758   1286 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW mSaRTLNAW I1M, P3A I147M, P149A OV observed variant Sequence This variant was seen in 1/12 untreated progressors. Migueles2003
52758   1287 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW kSaRTLNAW I1K, P3A I147K, P149A OV observed variant Sequence This variant was seen in 1/12 untreated progressors. Migueles2003
52758   1288 B     Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW lSPRTfNAW I1L, L6F I147L, L152F OV observed variant Sequence This variant was seen in 1/12 untreated progressors. Migueles2003
53832   1413 C     Gag 147 155 p24(15-23) 1228..1254 B57 ISPRTLNAW mSPRTLNAW I1M I147M E escape documented in this paper CD8 T-cell Elispot - IFNy, Sequence This is de novo variant seen in infant by week 33 of age. The index peptide was recognized, but not the variant. Pillay2005
53832   1414 C     Gag 147 155 p24(15-23) 1228..1254 B57 ISPRTLNAW lSPRTLNAW I1L I147L DR diminished response CD8 T-cell Elispot - IFNy, Sequence This is de novo variant seen in infant by week 33 of age. Both index peptide and the variant were recognized, but response to the variant was diminished. Pillay2005
55002 ISP 1789       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW raPRTLNAW I1R, S2A I147R, S148A NSF non-susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding None of the patients tested recognized the variant. Turnbull2006
55002 ISP 1790       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW mSPRTLNAW I1M I147M NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding Some patients recognized the variant, some did not. Turnbull2006
55002 ISP 1791       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW vSPRTLNAW I1V I147V NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding Some patients recognized the variant, some did not. Turnbull2006
55002 ISP 1792       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW ltPRTLNAW I1L, S2T I147L, S148T NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding Some patients recognized the variant, some did not. Turnbull2006
55002 ISP 1793       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW vtPRTLNAW I1V, S2T I147V, S148T NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding Some patients recognized the variant, some did not. Turnbull2006
55002 ISP 1794       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW ISaRTLNAW P3A P149A NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding Some patients recognized the variant, some did not. Turnbull2006
55002 ISP 1795       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW IaPRTLNAr S2A, W9R S148A, W155R NSF non-susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding None of the patients tested recognized the variant. Turnbull2006
55002 ISP 1796       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW lSPRTLNAW I1L I147L DR, SF diminished response, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding Some patients recognized the variant at the level of the index peptide, some had diminished response. Turnbull2006
56630 IW9 1980       Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW lSPRTLNAW I1L I147L E escape documented in this paper CD8 T-cell Elispot - IFNy, Intracellular cytokine staining, Sequence A simple but atypical pattern of escape was seen with this variant in one patient, CH77 where the variant completely replaced the index epitope. In patient CH58, no significant change with respect to selection in this epitope was detected. For CH58, positive ELISpot from the full proteome scan but with not statistical evidence for selection for change was seen. For CH77, known T cell response from the full proteome scan with evidence for variation and escape by positive ELISpot was seen. Goonetilleke2009
53832   2304 C     Gag 147 155 p24(15-23) 1228..1254 B57 {A}ISPRTLNAW {p}lSPRTLNAW I1L, --1P I147L, -146P OV observed variant Sequence A substitution proximal to the epitope and variant within the epitope was seen in infant I5 by week 33. Pillay2005
53648 ISW9 2324       Gag 147 155 p24(15-23) 1228..1254 B57, B*5801 {A}ISPRTLNAW {p}lSPRTLNAW I1L, A-1P I147L, A146P IE, P inferred escape, processing Sequence ISPRTLNAW was recognized more often in children than in adults, and was the most frequently recognized B57 epitope in children. Longitudinal sequencing of 2 HLA B57 children born to HLA B57-negative mothers and HIV-negative fathers showed variants of this epitope: {p}lSPRTLNAW, and lSPRTLNAW. In both cases the mother carried {A}ISPRTLNAW, confirming that the mutations arose under selection pressure in the children following vertical transmission. Response to the variants was not studied, but a processing escape was assumed. Feeney2005a
57415 ISW9 2360 B B B Gag 147 155 p24(15-23) 1228..1254 B*57 ISPRTLNAW lSPRTLNAW I2L I147L LE literature escape CD8 T-cell Elispot - IFNy, Sequence This 147L mutation was more common in progressors than controllers. Tang2010
57415 ISW9 2361 B B B Gag 147 155 p24(15-23) 1228..1254 B*57 {A}ISPRTLNAW {p}lSPRTLNAW A1P, I2L A146P, I147L OV observed variant Sequence This double mutation was seen in one progressor, CH-01 and one controller, CH-04. Tang2010
57415 ISW9 2362 B B B Gag 147 155 p24(15-23) 1228..1254 B*57 {A}ISPRTLNAW {p}ISPRTLNAW A1P A146P LE, P literature escape, processing Sequence This antigen processing escape, 146P, was more common in controllers than progressors. Tang2010
57258 IW9 2552 D, A1 A1 D Gag 147 155 p24(15-23) 1228..1254 B*57 ISPRTLNAW lSPRTLNAW I1L I147L SF susceptible form CD8 T-cell Elispot - IFNy Previously-documented Clade D ISPRTLNAW escape variant I147L was not selected against among B*57+ clade A1 subjects. These subjects responded similarly to 147I and 147L. McKinnon2009
57649 ISW9 2567       Gag 147 155 p24(15-23) 1228..1254 B*57 ISPRTLNAW lSPRTLNAW I1L I147L E escape documented in this paper Relative replication capacity assay Of 2 HLA-B57-positive early controllers both had, at the earliest time point tested, signature B57 mutations in Gag that impaired viral replication capacity: T242N in TSTLQEQIGW (TSnLQEQIGW) and I147L in ISPRTLNAW (lSPRTLNAW). Miura2010
58232   2799 B B B Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW lSPRTLNAW I1L I147L IE inferred escape Sequence 1/3 or 2/3 sequences of epitope ISPRTLNAW varied at 350 DFOSx to lSPRTLNAW and xSPRTLNAW, where X = l or s. Position 15 in the epitope is marked as being under selection to vary. Ferrari2011
58232   2800 B B B Gag 147 155 p24(15-23) 1228..1254 B*5701 ISPRTLNAW xSPRTLNAW I1X I147X IE inferred escape Sequence 1/3 or 2/3 sequences of epitope ISPRTLNAW varied at 350 DFOSx to xSPRTLNAW, since x = l or s, and another variant, lSPRTLNAW is found. Position 15 in the epitope is marked as being under selection to vary. Ferrari2011
58674 ISW9 3093 C C C Gag 147 155 p24(15-23) 1228..1254 B*5701, B*5702, B*5703, B*5801 {A}ISPRTLNAW {x}ISPRTLNAW A-1X A146X CE calculated escape CD8 T-cell Elispot - IFNy, Sequence ISW9 escapes at A146X, {x}ISPRTLNAW, are seen in ˜100% of HLA-B*5703 and -B*5702 positive subjects. Kloverpris2012
58674 ISW9 3094 C C C Gag 147 155 p24(15-23) 1228..1254 B*5701, B*5702, B*5703, B*5801 ISPRTLNAW xSPRTLNAW I2X I148X CE calculated escape CD8 T-cell Elispot - IFNy, Sequence ISW9 escapes at I147X, xSPRTLNAW, are seen in >75% of HLA-B*5703 and -B*5702 positive subjects. Kloverpris2012
58743   3131       Gag 147 155 p24(15-23) 1228..1254 B*57 ISPRTLNAW lSPRTLNAW I1L I147L NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Sequence Mutant epitope lSPRTLNAW is recognized only by subject ES38 as seen by EliSpot; though it is found in both ES38 and CP2 HIV-1. Buckheit2012
58746   3135       Gag 149 160 p24(17-28) 1234..1269   EKIRLRPGGKKKYKL EKIRLRPGGKKKYqL K14Q K162Q NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant EKIRLRPGGKKKYqL was detected in CP2 and ES2 HIV-1 sequences, but is only recognized by CTL from subject CP2. Buckheit2012
56141 TV9 80 B     Gag 151 159 p24(19-27) 1240..1266 A2 TLNAWVKVV TLNAWVKVi V9I V159I DR diminished response CD8 T-cell Elispot - IFNy, Chromium-release assay To identify immunogenically optimized epitopes for use in vaccines, mutants of TV9 were tested in transgenic mice. Natural TV9 mutants tested in transgenic HLA-A*02 mice showed the following responses - the common mutant V9I, TLNAWVKVi was less immunogenic and had low cross-reactivity. TLNAWVKaV (most cross-reactive) and TLNAWVKai were highly immunogenic and cross-reactive to the consensus. Blondelle2008
56141 TV9 81 B     Gag 151 159 p24(19-27) 1240..1266 A2 TLNAWVKVV TLNAWVKaV V8A V158A SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay To identify immunogenically optimized epitopes for use in vaccines, mutants of TV9 were tested in transgenic mice. Natural TV9 mutants tested in transgenic HLA-A*02 mice showed the following responses - the common mutant V9I, TLNAWVKVi was less immunogenic and had low cross-reactivity. TLNAWVKaV (most cross-reactive) and TLNAWVKai were highly immunogenic and cross-reactive to the consensus. Blondelle2008
56141 TV9 82 B     Gag 151 159 p24(19-27) 1240..1266 A2 TLNAWVKVV TLNAWVKai V8A, V9I V158A, V159I SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay To identify immunogenically optimized epitopes for use in vaccines, mutants of TV9 were tested in transgenic mice. Natural TV9 mutants tested in transgenic HLA-A*02 mice showed the following responses - the common mutant V9I, TLNAWVKVi was less immunogenic and had low cross-reactivity. TLNAWVKaV (most cross-reactive) and TLNAWVKai were highly immunogenic and cross-reactive to the consensus. Blondelle2008
55357 8L 1589       Gag 151 159 p24(19-27) 1240..1266 A*0201 TLNAWVKLV TLNAWVKLi V9I V159I OV observed variant   9I is the one known variant of epitope TV9. Schaubert2007
57650 TV9 2569       Gag 151 159 p24(19-27) 1240..1266 A*0201 TLNAWVKVV kINAWiKVV T1K, L2I, V6I T151K, L152I, V156I SF susceptible form Flow cytometric T-cell cytokine assay, HLA binding, TCR binding, Tetramer binding This is a mimic peptide shown to consistently activate cross-reactive and equally functional CTLs as measured by cytotoxicity, cytokine production and suppression of HIV replication in vitro. Schaubert2010
53593 Gag 8.4 56   B CRF02_AG Gag 153 163 p24(21-31) 1246..1278   NAWVKVVEEKA NAWVKViEEKA V7I V159I DR, SSF diminished response, subtype-specific susceptible form Intracellular cytokine staining, T-cell Elispot The B clade immune response to NAWVKVVEEKA gives a diminished response to the CRF02 variant NAWVKViEEKA, but does cross-react. Amara2005a
58387 Peptide 38 2917 C C B Gag 154 168 p24(22-36) 1249..1293   xAWVKVIEEKAFSPE nAWVKVvEEKAFSPE x1N, I7V x154N, I160V SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-B peptide 38, xAWVKVIEEKAFSPE, did not elicit a response from South African subjects carrying clade-C virus. Zembe2011
55068   213 B, C B C Gag 156 164 p24(24-32) 1255..1281 B*1503 VKVVEEKAF VKViEEKAF V4I V159I SSF subtype-specific susceptible form   VKVVEEKAF epitope is found in subtype B, while the variant is found in subtype C. Both are frequently targeted by B*1503 positive individuals. Frahm2006
55648   17 A, CRF02_AG, CRF01_AE A, AG AE Gag 158 172 p24(26-40) 1261..1305   VIEEKAFSPEVIPMF VvEEKgFnPEVIPMF I2V, A6G, S8N I159V, A163G, S165N SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy 1 subject responded to peptide VIEEKAFSPEVIPMF from subtypes A and CRF02_AG; and to peptide VvEEKgFnPEVIPMF from subtype CRF01_AE. Aidoo2008
58840 KF11 3181 B B B Gag 161 173 p24(29-41) 1270..1308 B*5701 KAFSPEVIPMF KAFSPEVIPMs F11S F171S OV observed variant Flow cytometric T-cell cytokine assay Epitope mutation, E|KAFSPEVIPMs|S, was seen for KF11 by 104 weeks post-infection in P1 who carried HLA alleles A*0101,A*0301,B*2705,B*5701. Norstrom2012
58840 KF11 3182 B B B Gag 161 173 p24(29-41) 1270..1308 B*5701 KAFSPEVIPMF KAFSPEVIPMt F11T F171T OV observed variant Flow cytometric T-cell cytokine assay Epitope mutation, E|KAFSPEVIPMt|S, was seen for KF11 by 168 weeks post-infection in P1 who carried HLA alleles A*0101,A*0301,B*2705,B*5701 and by 377 weeks post-infection in P6 who carried HLA alleles A*0301,A*2402,B*3501,B*5701. Norstrom2012
58840 KF11 3183 B B B Gag 161 173 p24(29-41) 1270..1308 B*5701 KAFSPEVIPMF KAFSPEiIPMF V7I V167I OV observed variant Flow cytometric T-cell cytokine assay Epitope mutation, E|KAFSPEiIPMF|S, was seen for KF11 by 168 weeks post-infection in P1 who carried HLA alleles A*0101,A*0301,B*2705,B*5701 and by 301 weeks post-infection in P6 who carried HLA alleles A*0301,A*2402,B*3501,B*5701. Norstrom2012
58840 KF11 3184 B B B Gag 161 173 p24(29-41) 1270..1308 B*5701 KAFSPEVIPMF KAsSPEVIPMF F3S F163S OV observed variant Flow cytometric T-cell cytokine assay Epitope mutation, E|KAFSPEVIPMF|S, was seen for KF11 by 301 weeks post-infection in P6 who carried HLA alleles A*0301,A*2402,B*3501,B*5701. Norstrom2012
53635 KF11 139 C     Gag 162 172 p24(30-40) 1273..1305 B*5703 KAFSPEVIPMF KnFSPEVIPMF A2N A163N NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy 5 variants of the epitope were observed: KAFSPEVIPMF, KnFSPEVIPMF, rAFSPEVIPMF, and KgFnPEVIPMF. Depending on the subject, different versions of these variants were more or less susceptible to their CD8+ T cells, i.e., one person's escape form was another person's susceptible form. Responses against KnFSPEVIPMF were strong but subdominant in subjects carrying KAFSPEVIPMF and KnFSPEVIPMF and there was little or no response in subjects carrying KgFnPEVIPMF. Currier2005
53635 KF11 140 C     Gag 162 172 p24(30-40) 1273..1305 B*5703 KAFSPEVIPMF rAFSPEVIPMF K1R K162R NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy 5 variants of the epitope were observed: KAFSPEVIPMF, KnFSPEVIPMF, rAFSPEVIPMF, and KgFnPEVIPMF. Depending on the subject, different versions of these variants were more or less susceptible to their CD8+ T cells, i.e., one person's escape form was another person's susceptible form. Responses against rAFSPEVIPMF were among maximal in subjects carrying KAFSPEVIPMF, KnFSPEVIPMF and rAFSPEVIPMF but there was little or no response in subjects carrying KgFnPEVIPMF. Currier2005
53635 KF11 141 C     Gag 162 172 p24(30-40) 1273..1305 B*5703 KAFSPEVIPMF KgFnPEVIPMF A2G, S4N A163G, S165N NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy 5 variants of the epitope were observed: KAFSPEVIPMF, KnFSPEVIPMF, rAFSPEVIPMF, and KgFnPEVIPMF. Depending on the subject, different versions of these variants were more or less susceptible to their CD8+ T cells, i.e., one person's escape form was another person's susceptible form. Responses against KgFnPEVIPMF were strong but subdominant in subjects carrying KAFSPEVIPMF and KnFSPEVIPMF. In subjects carrying KgFnPEVIPMF there was a strong response against the index peptide but little or no response against other peptides. Subject carrying provirus with rAFSPEVIPMF showed dramatic nonrecognition of KgFnPEVIPMF. Currier2005
55053   143   A, C, D A Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KgFnPEVIPMF A2G, S4N A163G, S165N SNSF, SSF subtype-specific non-susceptible form, subtype-specific susceptible form   KAFSPEVIPMF within peptide EKAFSPEVIPMFSAL from A consensus, C isolate and D isolate was recognized by 5/5 HLA B*5701/B*5703 carriers from subtype A Kenyan cohort. The variant KgFnPEVIPMF within peptide EKgFnPEVIPMFSAL from A isolate was recognized by 3 out 5 subjects that recognized KAFSPEVIPMF and not recognized by 2 subjects. Currier2006
54625 KF11 219 C C   Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KgFnPEVIPMF A2G, S4N A163G, S165N OV observed variant   Epitope highly variant in African cohort when restricted by B*5703 but highly conserved in B*5701 European cohort. Frater2007
54625 KF11 220 C C   Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KnFSPEVIPMF A2N A163N OV observed variant   Epitope highly variant in African cohort when restricted by B*5703 but highly conserved in B*5701 European cohort. Frater2007
54625 KF11 221 C C   Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KsFSPEVIPMF A2S A163S OV observed variant   Epitope highly variant in African cohort when restricted by B*5703 but highly conserved in B*5701 European cohort. Frater2007
54625 KF11 222 C C   Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KgFSPEVIPMF A2G A163G OV observed variant   Epitope highly variant in African cohort when restricted by B*5703 but highly conserved in B*5701 European cohort. Frater2007
54625 KF11 223 C C   Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KgFkPEVIPMF A2G, S4K A163G, S165K OV observed variant   Epitope highly variant in African cohort when restricted by B*5703 but highly conserved in B*5701 European cohort. Frater2007
54625 KF11 224 C C   Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KsFSPEtIPMF A2S, V7T A163S, V168T OV observed variant   Epitope highly variant in African cohort when restricted by B*5703 but highly conserved in B*5701 European cohort. Frater2007
52191 KAFS 347 A, B B A, AC Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KgFnPEVIPMF A2G, S4N A163G, S165N SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Tetramer binding Variant found in clades A and AC. B*5701 CTL clones recognized this variant and displayed similar levels of lytic activity as against the wt at time 0 but 50% of activity at 24h later. This variant was presented more efficiently by B*5703 than by B*5701. The variant reacted with 100% of CTLs but failed to induce significant IFN-gamma secretion in 2 of the patients, indicating that this variant is unable to activate all downstream effector functions. However, it induced IFN-gamma in some patients' PBMCs. Gillespie2002
52191 KAFS 348 A, B B A Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAlSPEVIPMF F3L F164L SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Tetramer binding Variant found in clade A. It was recognized by CTLs and induced lysis of peptide-pulsed targets. The variant induced IFN-gamma secretion in PBMCs from 5 patients and did not induce secretion in PBMCs from 1 patient. Gillespie2002
52191 KAFS 349 A, B B A Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFSPEVIPvF M10V M171V SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Tetramer binding Variant found in clade A. It was recognized by CTLs and induced lysis of peptide-pulsed targets. The variant induced IFN-gamma secretion in PBMCs from all patients. Gillespie2002
52191 KAFS 350 A, B B O Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFnPEiIPMF S4N, V7I S165N, V168I SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Tetramer binding Variant found in group O. It was recognized by CTLs and induced lysis of peptide-pulsed targets. The variant induced IFN-gamma secretion in PBMCs from 4 patients and did not induce secretion in PBMCs from 2 patients. Gillespie2002
52191 KAFS 351 A, B B AC Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFSPEiIPMF V7I V168I SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Tetramer binding Variant found in clade A/C. It was recognized by CTLs and induced lysis of peptide-pulsed targets. The variant induced IFN-gamma secretion in PBMCs from all patients. Gillespie2002
52191 KAFS 352 A, B B AC Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFSqEVIPMF P5Q P166Q DR, SSF diminished response, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Tetramer binding Variant found in clade A /C. It induced IFN-gamma production in 3/6 patients' PBMC but it demonstrated a diminished capacity to sensitize target cells for lysis. This variant was a weak ligand. Gillespie2002
52191 KAFS 353 A, B     Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF rgFSPEVIPMF K1R, A2G K162R, A163G OV observed variant   Variant found in one patient in 10/11 clones. Gillespie2002
52191 KAFS 354 A, B     Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF rgsSPEVIPMF K1R, A2G, F3S K162R, A163G, F164S OV observed variant   Variant found in one patient in 1/11 clones. Gillespie2002
53741 KAF 502       Gag 162 172 p24(30-40) 1273..1305 B57 KAFSPEVIPMF KvFSPEVIPMF A2V A163V OV observed variant   Variant was found in 2/5 B57+ individuals, but was always in a minor form. The frequency of the epitope mutation did not correlate with the percentage of IFN-gamma producing CTLs. Jansen2005a
53741 KAF 503       Gag 162 172 p24(30-40) 1273..1305 B57 KAFSPEVIPMF eAFSPEVIPMF K1E K162E OV observed variant   Variant was found in 1/5 B57+ individuals, but was always in a minor form. The frequency of the epitope mutation did not correlate with the percentage of IFN-gamma producing CTLs. Jansen2005a
53741 KAF 504       Gag 162 172 p24(30-40) 1273..1305 B57 KAFSPEVIPMF KtFSPEVIPMF A2T A163T OV observed variant   Variant was found in 1/5 B57+ individuals, but was always in a minor form. The frequency of the epitope mutation did not correlate with the percentage of IFN-gamma producing CTLs. Jansen2005a
53776 KF11 913 B, C     Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF KgFSPEVIPMF A2G A163G A, E, NSF HLA association, escape documented in this paper, non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Mutation A163G is suggested to be a result of selection pressure from the HLA-B*57 allele, and can be transmitted and stable in the absence of HLA-B*57. Experimental evidence indicated that the mechanism of escape was an increased off-rate; CTL recognition of KgFSPEVIPMF was ablated. 3% of HLA-B*57-positive subjects, 2% of HLA-B*5801-positive subjects carried this variant. Leslie2005a
52760 KAF11 1289 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KsFSPEVIPMF A2S A163S OV observed variant Sequence This variant was seen only in one non-progressor and one treated progressor. Index epitope KAF11 is immunodominant in several subjects and highly conserved. Migueles2003
52760 KAF11 1290 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KgFnPEVIPMF A2G, S4N A163G, S165N OV observed variant Sequence This variant was seen only in one untreated progressor. Migueles2003
55001 KAF 1797 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF rAFSPEVIPMF K1R K162R SF susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding This natural variant was recognized in all patients tested. Turnbull2006
55001 KAF 1798 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KnFSPEVIPMF A2N A163N NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding About half of patients tested recognized the variant, other patients had reduced or no response. Turnbull2006
55001 KAF 1799 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KgFSPEVIPMF A2G A163G SF susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding All patients recognized the variant at >60% of the response to the index peptide. Turnbull2006
55001 KAF 1800 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KAFSPEiIPMF V7I V168I SF susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding All patients recognized the variant at >60% of the response to the index peptide. Turnbull2006
55001 KAF 1801 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KAFnPEVIPMF S4N S165N NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding About half of patients tested recognized the variant, other patients had reduced or no response. Turnbull2006
55001 KAF 1802 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KgFnPEVIPMF A2G, S4N A163G, S165N NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding 2 patients had response about 80% of the response to the index peptide. Most patients had reduced or no response. Turnbull2006
55001 KAF 1803 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KAFnPEiIPMF S4N, V7I S165N, V168I NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding 1 patient had response comparable to the response to the index peptide. Most patients had reduced or no response. Turnbull2006
55001 KAF 1804 B     Gag 162 172 p24(30-40) 1273..1305 B*5701 KAFSPEVIPMF KAFSPgVIPMF E6G E167G NSF non-susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding None of the patients tested responded to this variant. Turnbull2006
55092 KF11 1885 B, C B, C B, C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KgFSPEVIPMF A2G A163G SNSF, SSF subtype-specific non-susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Intracellular cytokine staining, Sequence, Tetramer binding This variant is seen in both Clades B and C and binds HLA-B*5703. A162G variant in Clade C is detected significantly more frequently than in Clade B and is preferentially selected in context of HLA-B*5703. This A2G variant was recognized by HLA-B*5701- and -B*5703-expressing subjects. Yu2007a
55092 KF11 1886 B, C B, C B, C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KnFSPEVIPMF A2N A163N SNSF, SSF subtype-specific non-susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Intracellular cytokine staining, Sequence, Tetramer binding This variant is seen in both Clades B and C and binds HLA-B*5703 and -B*5701. A162N variant in Clade C is detected significantly more frequently than in Clade B and is preferentially selected in context of HLA-B*5703. This A2N variant was recognized by HLA-B*5701- and -B*5703-expressing subjects. Yu2007a
55092 KF11 1887 B, C B, C B, C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KsFSPEVIPMF A2S A163S OV observed variant Sequence This variant is seen in both Clades B and C and binds HLA-B*5703. A162S variant in Clade C is detected significantly more frequently than in Clade B and is preferentially selected in context of HLA-B*5703. Yu2007a
55092 KF11 1889 B, C B, C C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KgFnPEVIPMF A2G, S4N A163G, S165N DHB, SNSF, SSF diminished HLA binding or increased off-rate, subtype-specific non-susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Intracellular cytokine staining, Sequence, Tetramer binding This variant is seen only in Clade C and binds HLA-B*5703. S164N variant is seen most frequently and is preferentially selected in context of HLA-B*5703. This A2G-S4N variant was recognized by HLA-B*5701- but not by -B*5703-expressing subjects, though avidity of recognition was reduced. Yu2007a
55092 KF11 1890 B, C B, C C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KgFkPEVIPMF A2G, S4K A163G, S165K DHB, SNSF, SSF diminished HLA binding or increased off-rate, subtype-specific non-susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Intracellular cytokine staining, Sequence, Tetramer binding This variant is seen only in Clade C and binds HLA-B*5703. S164K variant is seen most frequently and is preferentially selected in context of HLA-B*5703. This A2G-S4K variant was recognized by HLA-B*5701- but not by -B*5703-expressing subjects, though avidity of recognition was reduced. Yu2007a
55092 KF11 1892 B, C B, C C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KsFSPEtIPMF A2S, V7T A163S, V168T OV observed variant Sequence This variant is seen only in Clade C and binds HLA-B*5703. Yu2007a
55092 KF11 1893 B, C B, C C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFSPEiIPMF V7I V168I SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, Intracellular cytokine staining, Sequence, Tetramer binding This variant is seen only in Clade C and binds HLA-B*5701. The V7I variant was recognized by HLA-B*5701- and -B*5703-expressing subjects. Yu2007a
55092 KF11 1894 B, C B, C B Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KsFSPEiIPMF A2S, V7I A163S, V168I OV observed variant Sequence This variant is seen only in Clade B and binds HLA-B*5703. Yu2007a
55092 KF11 1895 B, C B, C B, C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFnPEVIPMF S4N S165N OV observed variant Sequence This variant was seen only in non-HLA-B57 carriers, in both Clades B and C sequences. Yu2007a
55092 KF11 1896 B, C B, C C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFnPEiIPMF S4N, V7I S165N, V168I OV observed variant Sequence This variant was seen only in non-HLA-B57 carriers, and only in their Clade C sequences. Yu2007a
55092 KF11 1897 B, C B, C B, C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF rAFSPEVIPMF K1R K162R OV observed variant Sequence This variant was seen only in non-HLA-B57 carriers, in both Clades B and C sequences. Yu2007a
55092 KF11 1898 B, C B C Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFSPkVIPMF E6K E167K OV observed variant Sequence This variant was seen only in non-HLA-B57 carriers, and only in Clade C sequences. Yu2007a
55092 KF11 1900 B, C     Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAlSPEVIPMF F3L F164L SF susceptible form CD8 T-cell Elispot - IFNy, Sequence The F3L variant was recognized by HLA-B*5701- and -B*5703-expressing subjects. Yu2007a
55092 KF11 1901 B, C     Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFSPEVIPvF M10V M171V SF susceptible form CD8 T-cell Elispot - IFNy, Sequence The M10V variant was recognized by HLA-B*5701- and -B*5703-expressing subjects. Yu2007a
55092 KF11 1902 B, C     Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFSqEVIPMF P5Q P166Q NSF non-susceptible form CD8 T-cell Elispot - IFNy, Sequence The P5Q variant was not recognized by HLA-B*5701- and -B*5703-expressing subjects. Yu2007a
55092 KF11 2268 B, C C B Gag 162 172 p24(30-40) 1273..1305 B*5701, B*5703 KAFSPEVIPMF KAFSPEaIPMF V7A V168A OV observed variant Sequence This variant was seen only in non-HLA-B57 carriers, and only in Clade B sequences. Yu2007a
57416 KF11 2363 B B B Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF KnFSPEVIPMF A2N A163N DHB, LE diminished HLA binding or increased off-rate, literature escape CD8 T-cell Elispot - IFNy, Sequence Controller subject CH-22 had the A163X escape that has a fitness cost. CH-22 lacked the partially compensating mutation S165X, however. Variant A163N was recognized with a lower avidity than wild type KF11. Tang2010
57416 KF11 2364 B B B Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF rAFSPEiIPMF K1R, V7I K162R, V168I DHB, LE diminished HLA binding or increased off-rate, literature escape CD8 T-cell Elispot - IFNy, Sequence This rare escape was seen in subject CH-13, a controller. CH-13 also displayed a rare substitution in epitope TW10 (TSTLQEQIGW), suggesting that the two rare mutational pathways may be inter-dependent. Avidity of this variant, rAFSPEiIPMF, was much lower than that of wild type KF11. Tang2010
53776 KF11 3067 B, C     Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF KnFSPEVIPMF A2N A163N A, E, NSF HLA association, escape documented in this paper, non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant KnFSPEVIPMF (A163N) did not elicit response in EliSpot assays. 8% of HLA-B*57-positive subjects, 2% of HLA-B*5801-positive subjects, and 1% of HLA-B&57/5801-negative subjects carried this variant. Leslie2005a
53776 KF11 3068 B, C     Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF KgFnPEVIPMF A2G, S4N A163G, S165N A, E, NSF HLA association, escape documented in this paper, non-susceptible form CD8 T-cell Elispot - IFNy, Sequence For mutation A163G, S165N CTL recognition of KgFnPEVIPMF was ablated. 14% of HLA-B*57-positive subjects, 6% of HLA-B*5801-positive subjects, and 5% of HLA-B*57/5801-negative subjects carried this variant. Leslie2005a
53776 KF11 3069 B, C     Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF KgFkPEVIPMF A2G, S4K A163G, S165K A, DHB, E, NSF HLA association, diminished HLA binding or increased off-rate, escape documented in this paper, non-susceptible form CD8 T-cell Elispot - IFNy, Sequence For mutation A163G, S165K CTL recognition of KgFkPEVIPMF was ablated. 8% of HLA-B*57-positive subjects carried this variant. Leslie2005a
53776 KF11 3070 B, C     Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF KsFSPEtIPMF A2S, V7T A163S, V168T OV observed variant Sequence Variant KsFSPEtIPMF (A163S, S168T) was found in 3% of HLA-B*57-positive subjects. Leslie2005a
53776 KF11 3071 B, C     Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF KAFSPEiIPMF V7I V168I OV observed variant Sequence Variant KAFSPEiIPMF (V168I) was found in 4% of HLA-B*57-positive, and 7% of HLA-B*57/5802-negative subjects. Leslie2005a
53776 KF11 3072 B, C     Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF KAFnPEVIPMF S4N S165N OV observed variant Sequence Mutation S165N was found in 7% of HLA-B*57/5801-negative subjects. Leslie2005a
58684 KF11 3100 C C C Gag 162 172 p24(30-40) 1273..1305 B*5703 KAFSPEVIPMF KxFSPEVIPMF A2X A163X OV observed variant Sequence Mutation KxFSPEVIPMF was seen in > 50% of HLA-B*5703-positive subjects. Kloverpris2012
58684 KF11 3101 C C C Gag 162 172 p24(30-40) 1273..1305 B*5703 KAFSPEVIPMF KAFxPEVIPMF S4X S165X OV observed variant Sequence Mutation KAFxPEVIPMF was seen in > 30% of HLA-B*5703-positive subjects. Kloverpris2012
58741 KF11 3130       Gag 162 172 p24(30-40) 1273..1305 B*57 KAFSPEVIPMF{S} KAFSPEVIPMF{t} S+1T S173T LE, NSF, SF literature escape, non-susceptible form, susceptible form CD4 T-cell Elispot - IFNy, Sequence The S173T mutation to epitope KF11 is seen and recognized in HLA-B*57 individuals like ES38, but in this case was present in both ES38 as well as non-B*57-subject, CP2. Buckheit2012
54631 GAG-23 1956 B B C Gag 163 179 p24(31-47) 1276..1326   AFSPEVIPMFSALSEGA AFSPEVIPMFtALSEGA S11T S173T SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence This Clade C consensus synthetic peptide variant from an immunodominant region, differs from the immunodominant Clade B consensus at 1 amino acid (5.9%) and both were recognized by subtype-B-infected subjects. Zhao2007
57652   2571       Gag 164 172 p24(32-40) 1279..1305 Mamu A*01 FSPEVIPMF FnPEVIPMF S2N S165N SF susceptible form CD8 T-cell Elispot - IFNy T cells specific for FSPEVIPMF recognized equally strongly all tested epitope variants: FnPEVIPMF, FSPEiIPMF, qSPEVIPMF, FnPEiIPMF, FSPqVIPMF in rhesus macaques vaccinated with HIVconsv. Rosario2010
57652   2572       Gag 164 172 p24(32-40) 1279..1305 Mamu A*01 FSPEVIPMF FSPEiIPMF V5I V168I SF susceptible form CD8 T-cell Elispot - IFNy T cells specific for FSPEVIPMF recognized equally strongly all tested epitope variants: FnPEVIPMF, FSPEiIPMF, qSPEVIPMF, FnPEiIPMF, FSPqVIPMF in rhesus macaques vaccinated with HIVconsv. Rosario2010
57652   2573       Gag 164 172 p24(32-40) 1279..1305 Mamu A*01 FSPEVIPMF qSPEVIPMF F1Q F164Q SF susceptible form CD8 T-cell Elispot - IFNy T cells specific for FSPEVIPMF recognized equally strongly all tested epitope variants: FnPEVIPMF, FSPEiIPMF, qSPEVIPMF, FnPEiIPMF, FSPqVIPMF in rhesus macaques vaccinated with HIVconsv. Rosario2010
57652   2574       Gag 164 172 p24(32-40) 1279..1305 Mamu A*01 FSPEVIPMF FnPEiIPMF S2N, V5I S165N, V168I SF susceptible form CD8 T-cell Elispot - IFNy T cells specific for FSPEVIPMF recognized equally strongly all tested epitope variants: FnPEVIPMF, FSPEiIPMF, qSPEVIPMF, FnPEiIPMF, FSPqVIPMF in rhesus macaques vaccinated with HIVconsv. Rosario2010
57652   2575       Gag 164 172 p24(32-40) 1279..1305 Mamu A*01 FSPEVIPMF FnPEiIPMF S2N, V5I S165N, V168I SF susceptible form CD8 T-cell Elispot - IFNy T cells specific for FSPEVIPMF recognized equally strongly all tested epitope variants: FnPEVIPMF, FSPEiIPMF, qSPEVIPMF, FnPEiIPMF, FSPqVIPMF in rhesus macaques vaccinated with HIVconsv. Rosario2010
57652   2576       Gag 164 172 p24(32-40) 1279..1305 Mamu A*01 FSPEVIPMF FSPqVIPMF E4Q E167Q SF susceptible form CD8 T-cell Elispot - IFNy T cells specific for FSPEVIPMF recognized equally strongly all tested epitope variants: FnPEVIPMF, FSPEiIPMF, qSPEVIPMF, FnPEiIPMF, FSPqVIPMF in rhesus macaques vaccinated with HIVconsv. Rosario2010
169   355 B     Gag 167 175 p24(35-43) 1288..1314 A*2601 EVIPMFSAL EVIPMFaAL S7A S173A OV observed variant   14 of 70 sequences had a conservative change at this position, either to A or to T. Only one subtype B sequence had this epitope variant. Goulder1996b
169   356 B     Gag 167 175 p24(35-43) 1288..1314 A*2601 EVIPMFSAL EVIPMFtAL S7T S173T OV observed variant   14 of 70 sequences had a conservative change at this position, either to A or to T. Goulder1996b
53745   683 A, B, C, CRF01_AE, D     Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EVIPMFaAL S7A S173A E, TCR escape documented in this paper, TCR related mutation CD8 T-cell Elispot - IFNy Variant bound to A*2603 with equal affinity as the consensus form but could not be recognized by an EVIPMFSAL-specific T-cell clone, so it may mediate TCR escape Kawashima2005
53745   684 A, B, C, CRF01_AE, D A, B, CRF01_AE, D C Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EVIPMFtAL S7T S173T E, TCR escape documented in this paper, TCR related mutation CD8 T-cell Elispot - IFNy Variant bound to A*2603 with equal affinity as the consensus form but could not be recognized by an EVIPMFSAL-specific T-cell clone, so it may mediate TCR escape Kawashima2005
53745   685 A, B, C, CRF01_AE, D     Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL kVIPMFSAL E1K E167K DHB diminished HLA binding or increased off-rate CD8 T-cell Elispot - IFNy Variant did not bind to A*2603. Kawashima2005
53745   686 A, B, C, CRF01_AE, D   A Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EiIPMFSAL V2I V168I OV observed variant   Variant found in clade A from HIV sequence database. Kawashima2005
53745   687 A, B, C, CRF01_AE, D   A Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EVIPvFSAL M5V M171V OV observed variant   Variant found in clade A from HIV sequence database. Kawashima2005
53745   688 A, B, C, CRF01_AE, D   A Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL gVIPMFSAL E1G E167G OV observed variant   Variant found in clade A from HIV sequence database. Kawashima2005
53745   689 A, B, C, CRF01_AE, D   B Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EgIPMFSAL V2G V168G OV observed variant   Variant found in clade B from HIV sequence database. Kawashima2005
53745   690 A, B, C, CRF01_AE, D   CRF01_AE Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EVIPMFpAL S7P S173P OV observed variant   Variant found in clade E from HIV sequence database. Kawashima2005
53745   691 A, B, C, CRF01_AE, D   B Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EiIPMFaAL V2I, S7A V168I, S173A OV observed variant   Variant found in clade B from HIV sequence database. Kawashima2005
53745   692 A, B, C, CRF01_AE, D   B Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EmIPMFaAL V2M, S7A V168M, S173A OV observed variant   Variant found in clade B from HIV sequence database. Kawashima2005
53745   693 A, B, C, CRF01_AE, D   B Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EVIPMFttL S7T, A8T S173T, A174T OV observed variant   Variant found in clade B from HIV sequence database. Kawashima2005
53745   694 A, B, C, CRF01_AE, D   C Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EiIPMFtAL V2I, S7T V168I, S173T OV observed variant   Variant found in clade C from HIV sequence database. Kawashima2005
53745   695 A, B, C, CRF01_AE, D   C Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EeIPMFtAL V2E, S7T V168E, S173T OV observed variant   Variant found in clade C from HIV sequence database. Kawashima2005
53745   696 A, B, C, CRF01_AE, D   C Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EVIPiFtAL M5I, S7T M171I, S173T OV observed variant   Variant found in clade C from HIV sequence database. Kawashima2005
53745   697 A, B, C, CRF01_AE, D   A Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EVIPvFtAL M5V, S7T M171V, S173T OV observed variant   Variant found in clade A from HIV sequence database. Kawashima2005
53745   698 A, B, C, CRF01_AE, D   C Gag 167 175 p24(35-43) 1288..1314 A*2601, A*2603 EVIPMFSAL EiIPiFtAL V2I, M5I, S7T V168I, M171I, S173T OV observed variant   Variant found in clade C from HIV sequence database. Kawashima2005
58694 VL8 3107 B B B Gag 168 175 p24(36-43) 1291..1314 Cw*0102 VIPMSFAL VIPMtFAL S5T S172T A, DR, E HLA association, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy, Intracellular cytokine staining C-mut VIPMtFAL was the result of an S173T substitution in Gag epitope VIPMSFAL (VL8). A peptide containing VIPMtFAL escape was less well recognized than wt VL8 as proved by testing for γ-IFN and TNF-α production with intracellular cytokine staining (ICS) of a VL8-specific CTL cell line and its HLA-Cw*0102-transfected APC. Blais2012
54630 GAG-24 1958 B B C Gag 170 187 p24(38-55) 1297..1350   PMFSALSEGATPQDLNTM PMFtALSEGATPQDLNTM S4T S173T SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence This Clade C consensus synthetic peptide variant from an immunodominant region, differs from the immunodominant Clade B consensus at 1 amino acid (5.6%) and both were recognized by subtype-B-infected subjects. Zhao2007
178   172 A A B, C, D Gag 173 192 p24(41-60) 1306..1365 B*8101 SALSEGATPQDLNMMLNIVG SALSEGATPQDLNtMLNtVG M14T, I18T M186T, I190T OV observed variant   CTL responses in three individuals with non-clade B infections were studied, 2 with subtype A infections, 1 with subtype C -- their infections all originated in East Africa. This epitope is distinct in subtype A relative to subtypes B, C, and D which share the dominant sequence: SALSEGATPQDLNTMLNTVG. Dorrell1999
55229   801 B, CRF01_AE   CRF01_AE Gag 173 192 p24(41-60) 1306..1365   SALSEGATPQDLNTMLNTVG SALSEGATPQDLNmMLNiVG T14M, T18I T186M, T190I OV observed variant Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This was the infecting variant in CRF01_AE and it did not change over time. Kozaczynska2007
55229   802 B, CRF01_AE   B Gag 173 192 p24(41-60) 1306..1365   SALSEGATPQDLNTMLNTVG tALSEGATPQDLNTMLNTVG S1T S173T IE inferred escape Sequence Patient was superinfected with three strains, B1, B2 and CRF01_AE. This variant developed in B1 to include 92% of the viruses within 4 years, and in B2 to include 96% of the viruses within 3 years. Kozaczynska2007
55054   144       Gag 180 188 p24(48-56) 1327..1353 B*4202 TPQDLNMML TPQDLNtML M7T M186T SNSF, SSF subtype-specific non-susceptible form, subtype-specific susceptible form   TPQDLNMML within peptide EGATPQDLNMMLNIV from A consensus and A isolate was recognized by 4 HLA B*4202 carriers from subtype A Kenyan cohort. The variant TPQDLNtML within peptide EGATPQDLNtMLNtV from C and D isolates was recognized by only 1 out 4 subjects that recognized TPQDLNMML. Currier2006
1712   176 A A B, C, D Gag 180 188 p24(48-56) 1327..1353 B53 TPQDLNMML TPQDLNtML M7T M186T SNSF, TCR subtype-specific non-susceptible form, TCR related mutation CD8 T-cell Elispot - IFNy, Cytotoxicity assay, Tetramer binding TPQDLNMML was subtype A-specific with no cross-recognition of the subtype B, C, and D variant, TPQDLNTML, although the B/C/D variant bound more efficiently to B53 in vitro. Position 7 shows great positional variation in crystal structures of two HLA-B53 complexes, suggesting that variation here might significantly alter the position of the peptide in the binding groove and thus affect TCR interactions. Dorrell2001
54622 TL9 225 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPeDLNTML Q3E Q182E OV observed variant   Found in African cohort Frater2007
54622 TL9 226 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPsDLNsML Q3S, T7S Q182S, T186S OV observed variant   Found in African cohort Frater2007
54622 TL9 227 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPQDLNmML T7M T186M OV observed variant   Found in African cohort Frater2007
54622 TL9 228 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPsDLNTMf Q3S, L9F Q182S, L188F OV observed variant   Found in African cohort Frater2007
54622 TL9 229 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPQDLNaML T7A T186A OV observed variant   Found in African cohort Frater2007
54622 TL9 230 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPrDLNmML Q3R, T7M Q182R, T186M OV observed variant   Found in African cohort Frater2007
54622 TL9 231 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPaDLNTML Q3A Q182A OV observed variant   Found in African cohort Frater2007
54622 TL9 232 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPrDLNTML Q3R Q182R OV observed variant   Found in African cohort Frater2007
54622 TL9 233 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPgDLNTML Q3G Q182G OV observed variant   Found in African cohort Frater2007
54622 TL9 234 C C C Gag 180 188 p24(48-56) 1327..1353 B*8101 TPQDLNTML TPQDLNTfL M8F M187F OV observed variant   Found in African cohort Frater2007
54594   343 A, C, D C, D A Gag 180 188 p24(48-56) 1327..1353 B42, B7, B81 TPQDLNTML TPQDLNmML T7M T186M DR diminished response   The wild type epitope sequence was common to subtypes C and D, the variant to subtype A. CTL response in 56 individuals from Tanzania was strongest for subtype C peptide, and much lower for subtype A, due to point mutation effect. The response was also lower for subtype D, due to frame-of-epitope effect. Geldmacher2007
54192 TL9 916 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPQDLNsML T7S T186S E escape documented in this paper CD8 T-cell Elispot - IFNy Most common variant for B*4201, B*8101 and B*3910. The variant was less well recognized than the wt, or not recognized at all, by CTLs from B*8101 and B*4201 positive individuals. Leslie2006
54192 TL9 917 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPtDLNTML Q3T Q182T E escape documented in this paper CD8 T-cell Elispot - IFNy Variant found in B*8101, B*4201 and B*0702 positive patients. The variant was less well recognized than the wt, or not recognized at all, by CTLs from B*8101 and B*4201 positive individuals. Leslie2006
54192 TL9 918 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPsDLNTML Q3S Q182S E escape documented in this paper CD8 T-cell Elispot - IFNy Variant found in B*8101 positive patients. The variant was less well recognized than the wt, or not recognized at all, by CTLs from B*8101 and B*4201 positive individuals. Leslie2006
54192 TL9 919 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPpDLNTML Q3P Q182P OV observed variant   Variant found in B*4201 positive patients. Leslie2006
54192 TL9 920 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPaDLNTML Q3A Q182A E escape documented in this paper CD8 T-cell Elispot - IFNy Variant found in B*8101 and B*4201 positive patients. The variant was less well recognized than the wt, or not recognized at all, by CTLs from B*8101 and B*4201 positive individuals. Leslie2006
54192 TL9 921 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPvDLNTML Q3V Q182V OV observed variant   Variant found in B*4201 positive patients. Leslie2006
54192 TL9 922 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPhDLNTML Q3H Q182H OV observed variant   Variant found in B*4201 positive patients. Leslie2006
54192 TL9 923 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPQDLNmML T7M T186M E escape documented in this paper CD8 T-cell Elispot - IFNy Variant found in B*8101 and B*4201 positive patients. The variant was not recognized by CTLs from B*8101 and B*4201 positive individuals. Leslie2006
54192 TL9 924 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TsQDLNTML P2S P181S OV observed variant   Variant found in B*8101 and B*4201 positive patients. Leslie2006
54192 TL9 925 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPeDLNTML Q3E Q182E OV observed variant   Variant found in 8% of B*4201 positive patients. Leslie2006
54192 TL9 926 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPsDLNsML Q3S, T7S Q182S, T186S OV observed variant   Variant found in 6% of B*4201 positive patients. Leslie2006
54192 TL9 927 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPgDLNTML Q3G Q182G OV observed variant   Variant found in 2% of B*4201 positive patients. Leslie2006
54192 TL9 928 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML aPQDLNTMv T1A, L9V T180A, L188V OV observed variant   Variant found in 2% of B*4201 positive patients. Leslie2006
54192 TL9 929 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML nPQDLNTML T1N T180N OV observed variant   Variant found in 2% of B*4201 positive patients. Leslie2006
54192 TL9 930 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPsDLNTMf Q3S, L9F Q182S, L188F OV observed variant   Variant found in 2% of B*4201 positive patients. Leslie2006
54192 TL9 931 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPQDLyTML N6Y N185Y OV observed variant   Variant found in 2% of B*4201 positive patients. Leslie2006
54192 TL9 932 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPQDLNTfL M8F M187F OV observed variant   Variant found in 2% of B*4201, and 2% of B*0702 positive patients. Leslie2006
54192 TL9 933 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TPQDLNTvL M8V M187V OV observed variant   Variant found in 2% of B*0702 positive patients. Leslie2006
54192 TL9 934 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML TqQDLNpML P2Q, T7P P181Q, T186P OV observed variant   Variant found in 6% of B*3910 positive patients. Leslie2006
54192 TL9 935 C     Gag 180 188 p24(48-56) 1327..1353   TPQDLNTML aPQDLNTML T1A T180A OV observed variant   Variant found in 6% of B*3910 positive patients. Leslie2006
55736   1523 C     Gag 180 188 p24(48-56) 1327..1353 B*81 TPQDLNTML TPQDmNTML L5M L184M CE calculated escape CD8 T-cell Elispot - IFNy, Sequence Variants TPQDmNTML, TPQDyNTML, TPQDsNTML were resistant to CTL response, but associated with lower viral loads, suggesting a fitness cost to the mutation. Rousseau2008
55736   1524 C     Gag 180 188 p24(48-56) 1327..1353 B*81 TPQDLNTML TPQDsNTML L5S L184S CE calculated escape CD8 T-cell Elispot - IFNy, Sequence Variants TPQDmNTML, TPQDyNTML, TPQDsNTML were resistant to CTL response, but associated with lower viral loads, suggesting a fitness cost to the mutation. Rousseau2008
55736   1525 C     Gag 180 188 p24(48-56) 1327..1353 B*81 TPQDLNTML TPQDyNTML L5Y L184Y CE calculated escape CD8 T-cell Elispot - IFNy, Sequence Variants TPQDmNTML, TPQDyNTML, TPQDsNTML were resistant to CTL response, but associated with lower viral loads, suggesting a fitness cost to the mutation. Rousseau2008
58675 Gag-TL9 3113 C C C Gag 180 188 p24(48-56) 1327..1353 B*4201 TPQDLNTML TPxDLNTML Q3X Q182X E escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding, Sequence p24-TL9 mutation, TPxDLNTML, is selected in 21% HLA-B*4201 (75% have wt TL9), 15% HLA-B*4202 (82% have wt TL9) and 5% HLA-B*42-negative (89% have wt TL9) subjects. Mutant TPlDLNTML is designated as an escape by the authors when presented by HLA-B*4201. Kloverpris2012a
58813 TL9 3155 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...I...A} TPtDLNTML{...h...t} Q3T, I+35H, A+60T Q182T, I223H, A248T OV observed variant Sequence A mutation within TL9, Q182T had developed by 2 weeks post-infection , and putative compensatory mutations I223H and A248T had also developed by then in a B*8101-positive subject [Donor HLA = A*2601, A*8001, B*1801, B*8101, Cw*0202, Cw*0401; relatively high VL with CD4+ cell count increasing between years 3-4 post-infection] Ntale2012
58813 TL9 3156 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...I...A} TPsDLNTML{...h...t} Q3S, I+35H, A+60T Q182S, I223H, A248T OV observed variant Sequence A mutation within TL9, Q182S had developed by 32 weeks post-infection , and putative compensatory mutations I223H and A248T had also developed by then in a B*8101-positive subject [Donor HLA = A*2601, A*8001, B*1801, B*8101, Cw*0202, Cw*0401; relatively high VL with CD4+ cell count increasing between years 3-4 post-infection] Ntale2012
58813 TL9 3157 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...I} TPQDLNTML{...a} I+35A I223A OV observed variant Sequence A mutation outside TL9, I223A had developed by 56 weeks post-infection in a B*8101-positive subject [Donor HLA = A*3001, A*3303, B*5301, B*8101, Cw*0401, Cw*0401; after an initial 18-24 months of control, this subject had an increased VL and decreased CD4+ T cell counts] Ntale2012
58813 TL9 3158 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...I...I} TPsDLNTML{...a...v} Q3S, I+35A, I+68V Q182S, I223A, I256V OV observed variant Sequence A mutation within TL9, Q182S, had developed by 83 weeks post-infection, and putative compensatory mutations I223A and I26V had also developed by then in a B*8101-positive subject [Donor HLA = A*3001, A*3303, B*5301, B*8101, Cw*0401, Cw*0401; after an initial 18-24 months of control, this subject had an increased VL and decreased CD4+ T cell counts] Ntale2012
58813 TL9 3159 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 {E...}TPQDLNTML{...I} {d...}aPsDLNsML{...a} T1A, Q3S, E-3D, I+35A, T7S T180A, Q182S, E177D, I223A, T186S OV observed variant Sequence Mutations within TL9, E177D, T180A, Q182S had developed by 108 weeks post-infection, and putative compensatory mutations I223A had also developed by then in a B*8101-positive subject [Donor HLA = A*3001, A*3303, B*5301, B*8101, Cw*0401, Cw*0401; after an initial 18-24 months of control, this subject had an increased VL and decreased CD4+ T cell counts] Ntale2012
58813 TL9 3160 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 {E...}TPQDLNTML{...I} {d...}TPsDLNsML{...v} Q3S, E-3D, I+35V, T7S Q182S, E177D, I223V, T186S OV observed variant Sequence Mutations within TL9, E177D, Q182S had developed by 108 weeks post-infection, and putative compensatory mutations I223V had also developed by then in a B*8101-positive subject [Donor HLA = A*3001, A*3303, B*5301, B*8101, Cw*0401, Cw*0401; after an initial 18-24 months of control, this subject had an increased VL and decreased CD4+ T cell counts]. The very same set of mutations developed in a B*3910-positive subject too, by 9 weeks post-infection [Donor HLA = A*3001, A*4301, B*3901, B*4202, Cw*1203, Cw*1701; a controller of infection] Ntale2012
58813 TL9 3161 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 {E...}TPQDLNTML{...H...I} {d...}TPsDLNsML{...q...v} Q3S, E-3D, H+31Q, I+35V, T7S Q182S, E177D, H219Q, I223V, T186S OV observed variant Sequence Mutations within TL9, E177D, Q182S had developed by 108 weeks post-infection, and putative compensatory mutations H219Q, I223V had also developed by then in a B*3910-positive subject, by 85 weeks post-infection [Donor HLA = A*3001, A*4301, B*3901, B*4202, Cw*1203, Cw*1701; a controller of infection] Ntale2012
58813 TL9 3162 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...I...I} TPaDLNTML{...v...v} Q3A, I+35V, I+68V Q182A, I223V, I256V OV observed variant Sequence A mutation within TL9, Q182A had developed by 8 weeks post-infection, and putative compensatory mutations I223V and !256V had also developed by then in a B*3910-positive subject, weeks post-infection [Donor HLA = A*3001, A*4301, B*3901, B*4202, Cw*1203, Cw*1701; a controller of infection] Ntale2012
58813 TL9 3163 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...I...I} TPgDLNTML{...v...v} Q3G, I+35V, I+68V Q182G, I223V, I256V OV observed variant Sequence A mutation within TL9, Q182G had developed by 28 weeks post-infection, and putative compensatory mutations I223V and I256V had also developed by then in a B*3910-positive subject [Donor HLA = A*3001, A*4301, B*3901, B*4202, Cw*1203, Cw*1701; a controller of infection] Ntale2012
58813 TL9 3164 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...M} TPhDLNTML{...i} Q3H, M+62I Q182H, M250I OV observed variant Sequence A mutation within TL9, Q182H, had developed by 50 weeks post-infection, and a putative compensatory mutation, M250I, had also developed by then in a B*8101-positive subject [Donor HLA = A*3009, A*4301, B*5802, B*8101, Cw*0401, Cw*0401; this subject was a controller for the first 18-24 months and thereafter became a progressor]. Ntale2012
58813 TL9 3165 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...M} TPtDLNTML{...i} Q3T, M+62I Q182T, M250I OV observed variant Sequence A mutation within TL9, Q182T, had developed by 54 weeks post-infection, and a putative compensatory mutation, M250I, had also developed by then in a B*8101-positive subject [Donor HLA = A*3009, A*4301, B*5802, B*8101, Cw*0401, Cw*0401; this subject was a controller for the first 18-24 months and thereafter became a progressor]. Ntale2012
58813 TL9 3166 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...M} TPaDLNTML{...i} Q3A, M+62I Q182A, M250I OV observed variant Sequence A mutation within TL9, Q182A, had developed by 71 weeks post-infection, and a putative compensatory mutation, M250I, had also developed by then in a B*8101-positive subject [Donor HLA = A*3009, A*4301, B*5802, B*8101, Cw*0401, Cw*0401; this subject was a controller for the first 18-24 months and thereafter became a progressor]. Ntale2012
58813 TL9 3167 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...M} TPsDLNTML{...i} Q3S, M+62I Q182S, M250I OV observed variant Sequence A mutation within TL9, Q182S, had developed by 84 weeks post-infection, and a putative compensatory mutation, M250I, had also developed by then in a B*8101-positive subject [Donor HLA = A*3009, A*4301, B*5802, B*8101, Cw*0401, Cw*0401; this subject was a controller for the first 18-24 months and thereafter became a progressor]. Ntale2012
58813 TL9 3168 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML TPsDLNsML Q3S, T7S Q182S, T186S OV observed variant Sequence Mutations within TL9, Q182S and T186S had developed by 97 weeks post-infection in a B*8101-positive subject [Donor HLA = A*3009, A*4301, B*5802, B*8101, Cw*0401, Cw*0401; this subject was a controller for the first 18-24 months and thereafter became a progressor]. Ntale2012
58813 TL9 3169 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...A} TPsDLNsML{...t} Q3S, A+60T, T7S Q182S, A248T, T186S OV observed variant Sequence Mutations within TL9, Q182S and T186S had developed by 110 weeks post-infection, as well as a putative compensatory mutation at A248T in a B*8101-positive subject [Donor HLA = A*3009, A*4301, B*5802, B*8101, Cw*0401, Cw*0401; this subject was a controller for the first 18-24 months and thereafter became a progressor]. Ntale2012
58813 TL9 3170 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...I} TPtDLNTML{...v} Q3T, I+68V Q182T, I256V OV observed variant Sequence A mutation within TL9, Q182T, had developed by 53 weeks post-infection, and putative compensatory mutation I256V had also developed by then in a B*4201-positive subject. Ntale2012
58813 TL9 3171 C C C Gag 180 188 p24(48-56) 1327..1353 B*3910, B*8101 TPQDLNTML{...H...I...M} TPQDLNTMf{...q...v...i} H31Q, I35V, M62I, L9F H219Q, I223V, M250I, L188F OV observed variant Sequence A mutation within TL9, L188F had developed by 76 weeks post-infection, and putative compensatory mutations H219Q, I223V and M250I had also developed by then in a B*4201, Cw*0802-positive subject Ntale2012
53705   331 B, G     Gag 180 191 p24(48-59) 1327..1362 B58 TPQDLNQMLNTV TPQDLNtMLNTV Q7T Q186T OV observed variant   Cross-clade T cell responses are frequently induced in individuals infected with different HIV-1 clades. There was an inverse correlation between the height of responses and epitope sequence divergence. For Gag epitopes, the magnitude of the response was directly linked to the homology between HLA anchor residues. Geels2005
1676   677       Gag 183 191 p24(51-59) 1336..1362 B14 DLNMMLNIV DLNMtLNvV M5T, I8V M187T, I190V SF susceptible form CD8 T-cell Elispot - IFNy This epitope and the variant were recognized by 3/7 HIV infected women and by 4/4 HIV-exposed, persistently seronegative women. Kaul2001a
196   1543 B B A Gag 183 191 p24(51-59) 1336..1362 B*1402, Cw8 DLNTMLNTV DLNnMLNiV T4N, T8I T186N, T190I SF susceptible form Chromium-release assay One HEPS Kenyan subject cross-reacted to this B clade epitope but elicited a stronger reaction to the A clade form, DLNnMLNiV. Rowland-Jones1998
195   1556   B D Gag 183 191 p24(51-59) 1336..1362 B14, Cw8 DLNTMLNTV DLNmMLNiV T4M, T8I T186M, T190I OV observed variant Chromium-release assay 5/6 Kenyan HEPS subjects recognized this clade B epitope which differed from the clade D variant, DLNmMLNiV. RowlandJones1998b
54632 GAG-27 1959 B B C Gag 193 210 p24(61-78) 1366..1419   GHQAAMQMLKETINEEAA GHQAAMQMLKdTINEEAA E11D E203D SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence This Clade C consensus synthetic peptide variant from an immunodominant region, differs from the immunodominant Clade B consensus at 1 amino acid (5.6%) and both were recognized by subtype-B-infected subjects. Zhao2007
53188   121 C C B Gag 197 205 p24(65-73) 1378..1404 H-2d ANQMLKDTI ANQMLKeTI D7E D203E SSF subtype-specific susceptible form CD4 T-cell Elispot - IFNy, CD8 T-cell Elispot - IFNy, Cytokine production, Cytolytic LDH release assay A cross-clade response to the C clade epitope ANQMLKDTI was observed to the B clade version of this epitope, aNqmlkEti. 66% lysis was observed to the peptide carrying the C clade epitope, only 33% to the B clade variant. Chugh2004
55324 G 805 A, B, C A, C B Gag 197 205 p24(65-73) 1378..1404 H-2Kd AMQMLKDTI AMQMLKeTI D7E D203E DR diminished response CD8 T-cell Elispot - IFNy After immunization with Clades A or C vaccines, both containing the wt epitope, T cells responded well to the index epitope, but poorly to this variant. Larke2007
55324 G 806 A, B, C A, C B Gag 197 205 p24(65-73) 1378..1404 H-2Kd AMQMLKDTI AMQiLKDTI M4I M200I DR diminished response CD8 T-cell Elispot - IFNy After immunization with Clades A or C vaccines, both containing the wt epitope, T cells responded well to the index epitope, and intermediately to this variant. Larke2007
57936 G1 2665 A A A Gag 197 205 p24(65-73) 1378..1404 H-2Kd AMQMLKDTI AMefLKDTa Q3E, M4F, I9A Q199E, M200F, I205A DHB diminished HLA binding or increased off-rate HLA binding Artificially-produced mutant AMefLKDTa was created to abrogate the anchor residues of epitope AMQMLKDTI. Loss of HLA binding was confirmed. Im2011
55640   18 A, CRF01_AE A AE Gag 198 211 p24(66-79) 1381..1422   MQMLKDTINEEAAE MQMLKeTINEEAAE D6E D203E SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy 2 subjects responded to peptide MQMLKDTINEEAAE from subtype A and 1 of the 2 responded to peptide MQMLKeTINEEAAE of subtype CRF01_AE. Aidoo2008
54633 GAG-28 1960 B B C Gag 201 218 p24(69-86) 1390..1443   LKETINEEAAEWDRLHPV LKdTINEEAAEWDRLHPV E3D E203D SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence This Clade C consensus synthetic peptide variant from an immunodominant region, differs from the immunodominant Clade B consensus at 1 amino acid (5.6%) and both were recognized by subtype-B-infected subjects. Zhao2007
56301 EW10 159 B     Gag 203 212 p24(71-80) 1396..1425 A25 ETINEEAAEW ETINdEAAEW E5D E207D SF susceptible form Flow cytometric T-cell cytokine assay ETINEEAAEW, elicited a response in 1 patient with low viremia who also targeted Nef epitopes with high frequency. Patient had both the index epitope and the variant ETINdEAAEW which was recognized. Daucher2008
53681   332 A, B, D     Gag 203 212 p24(71-80) 1396..1425 B53, B58 ETINEEAAEW dTINEEAAEW E1D E203D OV observed variant   Cross-clade T cell responses are frequently induced in individuals infected with different HIV-1 clades. There was an inverse correlation between the height of responses and epitope sequence divergence. For Gag epitopes, the magnitude of the response was directly linked to the homology between HLA anchor residues. Geels2005
209   738       Gag 203 212 p24(71-80) 1396..1425 A*2501 ETINEEAAEW dTINEEAAEW E1D E203D OV observed variant   ETINEEAAEW is found in most B, D, and E subtype isolates while the variant is found in A and some D subtype sequences. Klenerman1996
54147 EW10 956 B     Gag 203 212 p24(71-80) 1396..1425 A*2501 ETINEEAAEW ETINdEAAEW E5D E207D DR diminished response CD8 T-cell Elispot - IFNy Amino acid site in the 5th position potentially experienced positive selection. Wt form of the epitope was 27 times better recognized than the variant, making the variant a partial escape. Liu2006
1713   2210 A A B, C, D Gag 203 212 p24(71-80) 1396..1425 B53 DTINEEAAEW eTINEEAAEW D1E D203E DR, SSF diminished response, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Cytotoxicity assay, Tetramer binding DTINEEAAEW was not subtype A-specific and there was cross-recognition, although diminished, of the subtype B, C, and D variant, ETINEEAAEW. Dorrell2001
53871   1870 B B A, B Gag 207 215 p24(75-83) 1408..1434 B*40 EEAAEWDRV EEAAEWDRl V9L V215L SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Autologous variant differed from the Strain B consensus, but was recognized. Yang2005
58783 p24Gag209-218 3146 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV AAEWDRmHPV L7M L215M A, DHB HLA association, diminished HLA binding or increased off-rate HLA binding Gag209-218-M, AAEWDRmHPV, binds HLA-Cw*0102 but at a decreased level. 2.9% sequences carried this variation. Fadda2012
58783 p24Gag209-218 3147 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV AAEWDRaHPV L7A L215A A HLA association HLA binding Gag209-218-A, AAEWDRaHPV, showed a significant increase in binding to HLA-Cw*0102. 0.9% of sequences carried this variant. Fadda2012
58783 p24Gag209-218 3148 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV AAEWDRqHPV L7Q L215Q A, DHB HLA association, diminished HLA binding or increased off-rate HLA binding Gag209-218-Q, AAEWDRqHPV, showed a slight decrease in binding to HLA-Cw*0102. 0.1% of sequences carried this variant. Fadda2012
58783 p24Gag209-218 3149 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV AAEWDRsHPV L7S L215S A HLA association HLA binding Gag209-218-S, AAEWDRsHPV, showed an increase in binding to HLA-Cw*0102. 0.1% of sequences carried this variant. Fadda2012
58783 p24Gag209-218 3150 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV AAEWDRtHPV L7T L215T A HLA association HLA binding Gag209-218-T, AAEWDRtHPV, showed a significant increase in binding to HLA-Cw*0102. 5.2% of sequences carried this variant. Fadda2012
58783 p24Gag209-218 3151 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV AAEWDRvHPV L7V L215V A HLA association HLA binding Gag209-218-V, AAEWDRvHPV, showed a significant increase in binding to HLA-Cw*0102. 16.3% of sequences carried this variant. Fadda2012
58783 p24Gag209-218 3152 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV AAEWDRiHPV L7I L215I A HLA association HLA binding Gag209-218-I, AAEWDRiHPV, showed an increase in binding to HLA-Cw*0102. 3.6% of sequences carried this variant. Fadda2012
58783 p24Gag209-218 3153 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV -AEWDRxHPV A1-, L7X A209-, L215X A, DHB HLA association, diminished HLA binding or increased off-rate HLA binding All sequences with mutations at position 7 and without the N-terminal Alanine were able to bind Cw*0102, but at reduced levels. Fadda2012
58783 p24Gag209-218 3154 B B B Gag 209 218 p24(77-86) 1414..1443   AAEWDRLHPV AAEWDRxHP- V10-, L7X V218-, L215X A, DHB HLA association, diminished HLA binding or increased off-rate HLA binding All sequences with mutations at position 7 and without the C-terminal Valine were unable to bind Cw*0102. Fadda2012
53421 AEW 1351       Gag 210 218 p24(78-86) 1417..1443 A2 AEWDRLHPV AEWgRLHPV D4G D213G OV observed variant CD8 T-cell Elispot - IFNy, Sequence, Tetramer binding Only 1/18 viral clones contained this variant sequence at the first time point tested after infection. Oxenius2004
53421 AEW 1352       Gag 210 218 p24(78-86) 1417..1443 A2 AEWDRLHPV AdWDRvHPV E2D, L6V E211D, L215V OV observed variant CD8 T-cell Elispot - IFNy, Sequence, Tetramer binding Only 1/18 viral clones contained this variant sequence at the first time point tested after infection. Oxenius2004
53870   1871 B B A, B Gag 210 218 p24(78-86) 1417..1443 B*40 AEWDRVHPV AEWDRlHPV V6L V215L SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Autologous variant differed from the Strain B consensus, but was recognized. Yang2005
53421 AEW 2302       Gag 210 218 p24(78-86) 1417..1443 A2 AEWDRLHPV AE*DRLHPV W3* W212* OV observed variant CD8 T-cell Elispot - IFNy, Sequence, Tetramer binding This index epitope sequence had variants at position 3 that were not specified in the paper. Only 2/18 viral clones contained variant sequences at the first time-point tested after infection. Oxenius2004
58728 DQ15 3128       Gag 213 227 p24(81-95) 1426..1470   DRLHPVHAGPIAPGQ DRvHPVHAGPIAPGQ L3V L215V SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Epitope DQ15 was seen to mutate to DRvHPVHAGPIAPGQ in subject CP1 but not in the controller, VC1. Subject CP1 recognizes DRvHPVHAGPIAPGQ as shown by EliSpot. Buckheit2012
53414 DRL 1353       Gag 213 232 p24(81-100) 1426..1485   DRLHPVHAGPAAPGQMREPR DRLHPVHAGPiAPGQMREPR A11I A223I DR diminished response CD8 T-cell Elispot - IFNy, Sequence, Tetramer binding Diminished response at higher peptide concentration, similar response at lower peptide concentration. Oxenius2004
214   1624   B B Gag 215 224 p24(83-92) 1432..1461 B55 VHPVHAGPIA lHPVHAGPvA V1L, I9V V215L, I223V SF susceptible form Chromium-release assay This naturally occurring, strain PH136 variant, was recognized by a Patient LWR CTL clone. Sipsas1997
214   1625   B B Gag 215 224 p24(83-92) 1432..1461 B55 VHPVHAGPIA lHPVHAGPIA V1L V215L SF susceptible form Chromium-release assay This naturally occurring, strain RF variant, was recognized by a Patient LWR CTL clone. Sipsas1997
214   1626   B B Gag 215 224 p24(83-92) 1432..1461 B55 VHPVHAGPIA lHPVHAGPIt V1L, A10T V215L, A224T SF susceptible form Chromium-release assay This naturally occurring, strain MN variant, was recognized by a Patient LWR CTL clone. Sipsas1997
214   1627   B B Gag 215 224 p24(83-92) 1432..1461 B55 VHPVHAGPIA lHPaqAGPIA V1L, V4A, H5Q V215L, V218A, H219Q SF susceptible form Chromium-release assay This naturally occurring, strain JH3 variant, was very poorly recognized by a Patient LWR CTL clone. Sipsas1997
57432 HA9 2472 C, D, A1 A1, C, D C, D Gag 216 224 p24(84-92) 1435..1461 B7 supertype HPVHAGPVA HPVqAGPVA H4Q H219Q NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patients 2295 (Caucasian female, experienced some treatment, autologous virus Clade C) and 2840 (African female, treated, autologous virus Clade D) continued to elicit response to variant HPVqAGPVA, but cells encountering this variant were not susceptible in patient 2632 (African female, experienced some treatment, autologous virus Clade A1). Hoof2010
57432 HA9 2473 C, D, A1 A1, C, D C, D Gag 216 224 p24(84-92) 1435..1461 B7 supertype HPVHAGPVA HPVHAGPiA V8I V223I NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patients 2295 (Caucasian female, experienced some treatment, autologous virus Clade C) and 2840 (African female, treated, autologous virus Clade D) continued to elicit response to variant HPVHAGPiA, but cells encountering this variant were not susceptible in patient 2632 (African female, experienced some treatment, autologous virus Clade A1). Hoof2010
57432 HA9 2474 C, D, A1 A1, C, D C, D Gag 216 224 p24(84-92) 1435..1461 B7 supertype HPVHAGPVA HPVHAGPip V8I, A9P V223I, A224P NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patients 2295 (Caucasian female, experienced some treatment, autologous virus Clade C) and 2840 (African female, treated, autologous virus Clade D) continued to elicit response to variant HPVHAGPip, but cells encountering this variant were not susceptible in patient 2632 (African female, experienced some treatment, autologous virus Clade A1). Hoof2010
57432 HA9 2475 C, D, A1 A1, C, D C, D Gag 216 224 p24(84-92) 1435..1461 B7 supertype HPVHAGPVA HPVHAGPVp A9P A224P NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patients 2295 (Caucasian female, experienced some treatment, autologous virus Clade C) and 2840 (African female, treated, autologous virus Clade D) continued to elicit response to variant HPVHAGPVp, but cells encountering this variant were not susceptible in patient 2632 (African female, experienced some treatment, autologous virus Clade A1). Hoof2010
57432 HA9 2476 C, D, A1 A1, C, D C, D Gag 216 224 p24(84-92) 1435..1461 B7 supertype HPVHAGPVA HPaHAGPVA V3A V218A NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patients 2295 (Caucasian female, experienced some treatment, autologous virus Clade C) and 2840 (African female, treated, autologous virus Clade D) continued to elicit response to variant HPaHAGPVA, but cells encountering this variant were not susceptible in patient 2632 (African female, experienced some treatment, autologous virus Clade A1). Hoof2010
57432 HA9 2477 C, D, A1 A1, C, D D Gag 216 224 p24(84-92) 1435..1461 B7 supertype HPVHAGPVA HPVaAGPVA H4A H219A NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patient 2840 (African female, treated, autologous virus Clade D) continued to elicit response to variant HPVaAGPVA, but cells encountering this variant were not susceptible in patients 2632 (African female, experienced some treatment, autologous virus Clade A1) and 2295 (Caucasian female, experienced some treatment, autologous virus Clade C). Hoof2010
57432 HA9 2478 C, D, A1 A1, C, D C, D Gag 216 224 p24(84-92) 1435..1461 B7 supertype HPVHAGPVA HPVHvGPVA A5V A220V NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patients 2295 (Caucasian female, experienced some treatment, autologous virus Clade C) and 2840 (African female, treated, autologous virus Clade D) continued to elicit response to variant HPVHvGPVA, but cells encountering this variant were not susceptible in patient 2632 (African female, experienced some treatment, autologous virus Clade A1). Hoof2010
57432 HA9 2479 C, D, A1 A1, C, D C, D Gag 216 224 p24(84-92) 1435..1461 B7 supertype HPVHAGPVA HPVHAaPVA G6A G221A NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patients 2295 (Caucasian female, experienced some treatment, autologous virus Clade C) and 2840 (African female, treated, autologous virus Clade D) continued to elicit response to variant HPVHAaPVA, but cells encountering this variant were not susceptible in patient 2632 (African female, experienced some treatment, autologous virus Clade A1). Hoof2010
55285   1506 B     Gag 219 233 p24(87-101) 1444..1488 A2 HAGPIAPGQMREPRG qAGPIAPGQMRdPRG H1Q, E12D H219Q, E230D OV observed variant Sequence This index epitope was conserved in the mother's viral strain but mutated in the daughter's isolate. Reinis2007
58388 Peptide 59 2919 C C C Gag 238 252 p24(106-120) 1501..1545   GTTSTLQEQIAWMTS GTTSTLQgQIAWMTS E8G E245G SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Chinese Clade-C peptide 59, GTTSTLQgQIAWMTS, did not elicit a response from South African subjects carrying clade-C virus. Zembe2011
58388 Peptide 59 2920 C C B Gag 238 252 p24(106-120) 1501..1545   xGTTSTLQEQIAWMT aGTTSTLQEQIgWMT x1A, A12G x238A, A249G SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-B peptide 59, aGTTSTLQEQIgWMT, did not elicit a response from South African subjects carrying clade-C virus. Zembe2011
58388 Peptide 59 2921 C C A Gag 238 252 p24(106-120) 1501..1545   GTTSTLQEQIAWMTS GTTSTLQEQIgWMTS A11G A248G SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-A peptide 59, GTTSTLQEQIgWMTS, did not elicit a response from South African subjects carrying clade-C virus. Zembe2011
58842 TW10 3188 B B B Gag 239 250 p24(107-118) 1504..1539 B*5701 TSTLQEQIGW TSTLrEQIGW Q5R Q243R OV observed variant Sequence Epitope mutation, T|TSTLrEQIGW|M, was seen for TW10 by the first sampling 13 weeks post-infection in P1 who carried HLA alleles A*0101,A*0301,B*2705,B*5701. Norstrom2012
58842 TW10 3189 B B B Gag 239 250 p24(107-118) 1504..1539 B*5701 TSTLQEQIGW TSTLQEQIeW G9E G247E OV observed variant Sequence Epitope mutation, T|TSTLQEQIeW|M, was seen for TW10 by the first sampling 13 weeks post-infection in P1 who carried HLA alleles A*0101,A*0301,B*2705,B*5701 and at 13 weeks post-infection in P5 who carried HLA alleles A*0101,A*0101,B*0801,B*5701. Norstrom2012
58842 TW10 3190 B B B Gag 239 250 p24(107-118) 1504..1539 B*5701 TSTLQEQIGW TSnLQEQIGW T3N T241N OV observed variant Sequence Most common epitope mutation, T|TSnLQEQIGW|M, was seen for TW10 by the first sampling 13 weeks post-infection in P1 who carried HLA alleles A*0101,A*0301,B*2705,B*5701; by 18 weeks post-infection in P2 who carried HLA alleles A*0101,A*0301,B*2705,B*5701; by 13 weeks post-infection in P3 who carried HLA alleles A*2402,A*3201,B*4002,B*5701; by 11 weeks post-infection in P4 who carried HLA alleles A*0101,A*0201,B*5101,B*5701 and by 10 weeks post-infection in P6 who carried HLA alleles A*0301,A*2402,B*3501,B*5701. Norstrom2012
58842 TW10 3192 B B B Gag 239 250 p24(107-118) 1504..1539 B*5701 TSTLQEQIGW TSsLQEQIGW T3S T241S OV observed variant Sequence Epitope mutation, T|TSsLQEQIGW|M, was seen for TW10 by the first sampling 18 weeks post-infection in P2 who carried HLA alleles A*0101,A*0301,B*2705,B*570. Norstrom2012
58842 TW10 3193 B B B Gag 239 250 p24(107-118) 1504..1539 B*5701 TSTLQEQIGW TSnLQEQIrW T3N, G9R T241N, G247R OV observed variant Sequence Most common epitope mutation, T|TSnLQEQIrW|M, was seen for TW10 by 109 weeks post-infection in P2 who carried HLA alleles A*0101,A*0301,B*2705,B*5701. Norstrom2012
58842 TW10 3194 B B B Gag 239 250 p24(107-118) 1504..1539 B*5701 TSTLQEQIGW TSnLQEQIaW T3N, G9A T241N, G247A OV observed variant Sequence Most common epitope mutation, T|TSnLQEQIaW|M, was seen for TW10 by 45 weeks post-infection in P3 who carried HLA alleles A*2402,A*3201,B*4002,B*5701; by 11 weeks post-infection in P4 who carried the HLA alleles A*0101,A*0201,B*5101,B*5701; and by 144 weeks post-infection in P5 who carried the HLA alleles A*0101,A*0101,B*0801,B*5701. Norstrom2012
58842 TW10 3195 B B B Gag 239 250 p24(107-118) 1504..1539 B*5701 TSTLQEQIGW TSnLQEQItW T3N, G9R T241N, G247R OV observed variant Sequence Most common epitope mutation, T|TSnLQEQIrW|M, was seen for TW10 by 195 weeks post-infection in P2 who carried HLA alleles A*0101,A*0301,B*2705,B*5701. Norstrom2012
58842 TW10 3196 B B B Gag 239 250 p24(107-118) 1504..1539 B*5701 TSTLQEQIGW TSTLQEQIaW G9A G247A OV observed variant Sequence Most common epitope mutation, T|TSTLQEQIaW|M, was seen for TW10 by 13 weeks post-infection in P3 who carried HLA alleles A*2402,A*3201,B*4002,B*5701. Norstrom2012
53203 TW10 33 B     Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSnLQEQIGW T3N T242N E escape documented in this paper CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay The acute immunodominant response was to TSTLQEQIGW. The response declined following viral escape to TSnLQEQIGW by day 64. Allen2004
53640 TW10 197       Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay TW10 was found to be more frequently recognized by HLA B57-positive adults than by HLA B57-positive children. All 14 children carried mutations of this epitope which are usually escape mutations in adults. However, majority of children (9/13) exhibited a robust response to autologous variants, while recognizing wild type epitope weakly or not at all. TSnLQEQIaW was the most common autologous variant (recognized by children), other recognized autologous variants included TSTLQEQIaW, TSnLQEQItW, TSnLaEQIaW. Feeney2005a
53640 TW10 198       Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSTLQEQIaW G9A G248A SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay TW10 was found to be more frequently recognized by HLA B57-positive adults than by HLA B57-positive children. All 14 children carried mutations of this epitope which are usually escape mutations in adults. However, majority of children (9/13) exhibited a robust response to autologous variants, while recognizing wild type epitope weakly or not at all. TSnLQEQIaW was the most common autologous variant (recognized by children), other recognized autologous variants included TSTLQEQIaW, TSnLQEQItW, TSnLaEQIaW. Feeney2005a
53640 TW10 199       Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSnLQEQItW T3N, G9T T242N, G248T SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay TW10 was found to be more frequently recognized by HLA B57-positive adults than by HLA B57-positive children. All 14 children carried mutations of this epitope which are usually escape mutations in adults. However, majority of children (9/13) exhibited a robust response to autologous variants, while recognizing wild type epitope weakly or not at all. TSnLQEQIaW was the most common autologous variant (recognized by children), other recognized autologous variants included TSTLQEQIaW, TSnLQEQItW, TSnLaEQIaW. Feeney2005a
53640 TW10 200       Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSnLaEQIaW T3N, Q5A, G9A T242N, Q244A, G248A SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay TW10 was found to be more frequently recognized by HLA B57-positive adults than by HLA B57-positive children. All 14 children carried mutations of this epitope which are usually escape mutations in adults. However, majority of children (9/13) exhibited a robust response to autologous variants, while recognizing wild type epitope weakly or not at all. TSnLQEQIaW was the most common autologous variant (recognized by children), other recognized autologous variants included TSTLQEQIaW, TSnLQEQItW, TSnLaEQIaW. Feeney2005a
54619 TW10 235 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*58 TSTLQEQIGW TSnLQEQIGW T3N T242N CE calculated escape   The variant was more often found in HLA-matched than in HLA-unmatched patients, indicating that some favourable HLA alleles induce strong pressure, resulting in escape variants with high fitness cost and low viral loads. Frater2007
54619 TW10 236 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*58 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A CE calculated escape   The variant was more often found in HLA-matched than in HLA-unmatched patients, indicating that some favourable HLA alleles induce strong pressure, resulting in escape variants with high fitness cost and low viral loads. Frater2007
54619 TW10 237 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*58 TSTLQEQIGW TSTpQEQIGW L4P L243P OV observed variant   Found in European cohort. Frater2007
54619 TW10 238 B     Gag 240 249 p24(108-117) 1507..1536 B*57, B*58 TSTLQEQIGW TSnLQEQIrW T3N, G9R T242N, G248R CE calculated escape   This variant was more often found in HLA-B*5703 and HLA-B*5801 patients. Frater2007
54621 TW10 239 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSnLQEQInW T3N, A9N T242N, A248N OV observed variant   Found in African and European cohort Frater2007
54621 TW10 240 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSnLQEQIAW T3N T242N CE calculated escape   This variant was more often found in HLA-B*5703 and HLA-B*5801 patients. Frater2007
54621 TW10 241 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSnLQEQItW T3N, A9T T242N, A248T CE calculated escape   This variant was more often found in HLA-B*5703 and HLA-B*5801 patients. Frater2007
54621 TW10 243 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSnLQEQvAW T3N, I8V T242N, I247V CE calculated escape   This variant was more often found in HLA-B*5703 patients. Frater2007
54621 TW10 244 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSnLaEQIAW T3N, Q5A T242N, Q244A CE calculated escape   This variant was more often found in HLA-B*5703 patients. Frater2007
54621 TW10 245 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSnLQEQIgW T3N, A9G T242N, A248G CE calculated escape   This variant was more often found in HLA-B*5703 and HLA-B*5801 patients. Frater2007
54621 TW10 246 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSnLgEQIAW T3N, Q5G T242N, Q244G CE calculated escape   This variant was more often found in HLA-B*5703 patients. Frater2007
54621 TW10 247 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSTpQEQIAW L4P L243P OV observed variant   Found in African B*5801 cohort Frater2007
54621 TW10 248 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSTtQEQIAW L4T L243T OV observed variant   Found in African cohort Frater2007
54621 TW10 249 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSsLQEQIAW T3S T242S OV observed variant   Found in African cohort Frater2007
54621 TW10 250 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSTLQEQIrW A9R A248R OV observed variant   Found in European cohort Frater2007
54621 TW10 251 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSTLaEQIAW Q5A Q244A OV observed variant   Found in African cohort Frater2007
54621 TW10 252 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSTLQEQvAW I8V I247V OV observed variant   Found in African cohort Frater2007
54621 TW10 253 C     Gag 240 249 p24(108-117) 1507..1536 B*5703, B*5801 TSTLQEQIAW TSTLQEQmAW I8M I247M OV observed variant   Found in African B*5703 cohort Frater2007
53214 TW10 395       Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSnLQEQIGW T3N T242N E escape documented in this paper   This escape variant occurs early in 75% of HLA-B*5801 and B57 positive individuals. Transmission of the variant to B*5801 and B57 negative individuals results in reversion to wt. Goulder2004
53214 TW10 396       Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSTLQEQIaW G9A G248A E escape documented in this paper   This variant occurs in one third of HLA-B*5801 and B57 positive individuals. Transmission of the variant to B*5801 and B57 negative individuals does not result in reversion to wt, indicating little fitness cost of the escape mutation. Goulder2004
53214 TW10 397       Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A E escape documented in this paper   This variant occurs in one third of HLA-B*5801 and B57 positive individuals. Transmission of the variant to B*5801 and B57 negative individuals results in reversion to wt at position 3 but not in position 9. Goulder2004
53047 TW10 886 B, C C B, C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQIAW T3N T242N DHB, DR, E diminished HLA binding or increased off-rate, diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy Variant shown to be an escape mutant correlated with HLA-B57 and HLA-B5801 alleles, and is never found in HLA-B57 and HLA-B5801 negative individuals. Variant was recognized to a lesser extent by CTLs than the wt epitope in clade C but the opposite is true in clade B. The variant can be transmitted to HLA-B57/B5801 negative individuals, but reverts to wild-type in those. Site under positive selection pressure. Leslie2004
53047 TW10 887 B, C C B, C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQIgW A9G A248G DR, SF diminished response, susceptible form CD8 T-cell Elispot - IFNy The most common form of the epitope in the B clade. Here, the variant is recognized by CTLs. In clade-C patients, this variant is weakly associated with HLA-B57 and is recognized to a lesser extent than the clade-C wt epitope, which has an A in this position. Leslie2004
53047 TW10 888 B, C C B, C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQIgW T3N, A9G T242N, A248G DR, E diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy This variant is either not recognized at all, or recognized to a lesser extent, by CTLs of patients infected with either clade B or clade C. The second A/G escape mutation is maintained after transmission. Leslie2004
53047 TW10 889 B, C C B, C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLaEQIAW T3N, Q5A T242N, Q244A OV observed variant   Variant found in HLA-B57 positive individuals in both clades B and C. Leslie2004
53047 TW10 890 B, C C B, C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQItW T3N, A9T T242N, A248T OV observed variant   Variant found in HLA-B57 and HLA-B5801 positive individuals in both clades B and C. Leslie2004
53047 TW10 891 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQvAW T3N, I8V T242N, I247V OV observed variant   Variant found in HLA-B57 positive individuals in clade C. Leslie2004
53047 TW10 892 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQmAW I8M I247M OV observed variant   Variant found in HLA-B57 positive individuals in clade C. Leslie2004
53047 TW10 893 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQmtW I8M, A9T I247M, A248T OV observed variant   Variant found in HLA-B57 positive individuals in clade C. Leslie2004
53047 TW10 894 B, C C B, C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQItW A9T A248T OV observed variant   Variant found in HLA-B57, HLA-B5801, and other alleles, positive individuals in both clades B and C. Leslie2004
53047 TW10 895 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQIiW A9I A248I OV observed variant   Variant found in HLA-B57 positive individuals in clade C. Leslie2004
53047 TW10 896 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQIqW A9Q A248Q OV observed variant   Variant found in HLA-B57 and HLA-B5801 positive individuals in clade C. Leslie2004
53047 TW10 897 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQvAW I8V I247V OV observed variant   Variant found in HLA-B57 positive individuals in clade C and in individuals with other alleles in clade C. Leslie2004
53047 TW10 898 B, C C B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTpQEQIgW L4P, A9G L243P, A248G OV observed variant   Variant found in HLA-B5801 positive individuals in clade C and in individuals with other alleles in clade B. Leslie2004
53047 TW10 899 B, C C B, C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSsLQEQIAW T3S T242S OV observed variant   Variant found in HLA-B5801 positive individuals in clade C and in individuals with other alleles in both clades B and C. Leslie2004
53047 TW10 900 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLaEQIAW Q5A Q244A OV observed variant   Variant found in HLA-B57 and HLA-B5801 positive individuals in clade C. Leslie2004
53047 TW10 901 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQInW T3N, A9N T242N, A248N OV observed variant   Variant found in HLA-B5801 positive individuals in clade C. Leslie2004
53047 TW10 902 B, C C B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQIqW T3N, A9Q T242N, A248Q OV observed variant   Variant found in HLA-B57 positive individuals in clade B. Leslie2004
53047 TW10 903 B, C C B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLaEQIgW T3N, Q5A, A9G T242N, Q244A, A248G OV observed variant   Variant found in HLA-B57 positive individuals in clade B. Leslie2004
53047 TW10 904 B, C C B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQIdW A9D A248D OV observed variant   Variant found in HLA-B57 positive individuals in clade B. Leslie2004
53047 TW10 905 B, C C B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSThQEQIgW L4H, A9G L243H, A248G OV observed variant   Variant found in HLA-B57 positive individuals in clade B. Leslie2004
53047 TW10 906 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQvdW I8V, A9D I247V, A248D OV observed variant   Variant found in individuals with other alleles than HLA-B57 and HLA-B5801 in clade C. Leslie2004
53047 TW10 907 B, C C B, C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQvtW I8V, A9T I247V, A248T OV observed variant   Variant found in individuals with other alleles than HLA-B57 and HLA-B5801 in both clades B and C. Leslie2004
53047 TW10 908 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQdQIAW E6D E245D OV observed variant   Variant found in individuals with other alleles than HLA-B57 and HLA-B5801 in clade C. Leslie2004
53047 TW10 909 B, C C B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQIeW A9E A248E OV observed variant   Variant found in individuals with other alleles than HLA-B57 and HLA-B5801 in clade B. Leslie2004
53047 TW10 910 B, C C B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTaQEQIgW L4A, A9G L243A, A248G OV observed variant   Variant found in individuals with other alleles than HLA-B57 and HLA-B5801 in clade B. Leslie2004
53047 TW10 911 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQIeW T3N, A9E T242N, A248E OV observed variant   Variant found in clade C. Leslie2004
53047 TW10 912 B, C C C Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQmAW T3N, I8M T242N, I247M OV observed variant   Variant found in clade C. Leslie2004
53387 gag 240-9 1012   B HIV-2 Gag 240 249 p24(108-117) 1507..1536 B57, B58 TSTLQEQIGW TSTveEQIqW L4V, Q5E, G9Q L243V, Q244E, G248Q SNSF, SSF subtype-specific non-susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy The HIV-2 variant of this epitope. 5/6 HIV-2 infected individuals could recognize both the HIV-1 and HIV-2 peptides, while 0/5 HIV-1 infected patients that could react with the HIV-1 peptide could also react with the HIV-2 peptide. Lopes2003
53387 gag 240-9 1013   B A Gag 240 249 p24(108-117) 1507..1536 B57, B58 TSTLQEQIGW TSTLQEQIaW G9A G248A DR, SNSF, SSF diminished response, subtype-specific non-susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy The clade A variant of this epitope. The variant resulted in significant reduction of CTL recognition in HIV-1 individuals, but was recognized by CTLs from HIV-2 infected patients. Lopes2003
54535 TW10 1022 B B A Gag 240 249 p24(108-117) 1507..1536 B57, B58 TSTLQEQIGW TSTpQEQIGW L4P L243P SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy No cross-recognition is seen with this A-clade variant. This A-clade variant contains a non-conservative change at position 4 to TSTpQEQIGW. Malhotra2007
54535 TW10 1023 B B C Gag 240 249 p24(108-117) 1507..1536 B57, B58 TSTLQEQIGW TSTLQEQIaW G9A G248A SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy Cross-recognition is seen only to the C-clade variant. This C-clade variant has a semi-conservative substitution at position 9 to TSTLQEQIaW. Reduced avidity was seen with this variant. Malhotra2007
54216 TW10 1070   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLaEQIaW T3N, Q5A, G9A T242N, Q244A, G248A OV observed variant Sequence This triple variant was found in 1/80 HLA-B*57/58 subjects infected by Clade B HIV-1, and in 0/239 HLA-B*57/5801 negative subjects. Martinez-Picado2006
54216 TW10 1071   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A E escape documented in this paper CD8 T-cell Elispot - IFNy, Previously reported in the literature, Sequence This previously suggested escape, a double variant was found in 30/80 HLA-B*57/58 subjects infected by Clade B HIV-1, but only in 1/239 HLA-B*57/5801 negative subjects. It abrogates recognition completely at low peptide concentrations. Martinez-Picado2006
54216 TW10 1072   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQItW T3N, G9T T242N, G248T OV observed variant Sequence This double variant was found in 4/80 HLA-B*57/58 subjects, but in none of 107 HLA-B*57/5801 negative subjects infected with Clade B HIV-1. Martinez-Picado2006
54216 TW10 1073   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQIqW T3N, G9Q T242N, G248Q OV observed variant Sequence This double variant was found in 3/80 HLA-B*57/58 subjects infected with Clade B HIV-1, but in no HLA-B*57/5801 negative subjects. Martinez-Picado2006
54216 TW10 1074   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLsEQIaW T3N, Q5S, G9A T242N, Q244S, G248A OV observed variant Sequence This triple variant was found in 1/80 HLA-B*57/58 subjects infected with Clade B HIV-1, and in no HLA-B*57/5801 negative subjects. Martinez-Picado2006
54216 TW10 1075   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQvaW T3N, I8V, G9A T242N, I247V, G248A OV observed variant Sequence This triple variant was found in 1/80 HLA-B*57/58 subjects infected with Clade B HIV-1, and in no HLA-B*57/5801 negative subjects. Martinez-Picado2006
54216 TW10 1076   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TtnLQEQIaW S2T, T3N, G9A S241T, T242N, G248A OV observed variant Sequence This triple variant was found in 1/80 HLA-B*57/58 subjects infected with Clade B HIV-1, and in no HLA-B*57/5801 negative subjects. Martinez-Picado2006
54216 TW10 1077   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSThQEQIaW L4H, G9A L243H, G248A OV observed variant Sequence This double variant was found in 1/80 HLA-B*57/58 subjects infected with Clade B HIV-1, and in no HLA-B*57/5801 negative subjects. Martinez-Picado2006
54216 TW10 1078   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSTLQEQIaW G9A G248A DR diminished response CD8 T-cell Elispot - IFNy, Previously reported in the literature, Sequence This variant was found in 6/80 HLA-B*57/58 subjects, but only in 17/107 HLA-B*57/5801 negative subjects infected with Clade B HIV-1. It arises commonly and at no cost to the virus and is readily transmitted to persistence in restricting HLA negative subjects, is not correlated with compensations and increases viral infectivity. It is however, relatively ineffective as an escape with only partial loss of recognition. Martinez-Picado2006
54216 TW10 1079   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSTLQEQIdW G9D G248D OV observed variant Sequence This variant was found in 1/68 HLA-B*57 subjects, and in 0/107 HLA-B*57/5801 negative subjects infected with Clade B HIV-1. Martinez-Picado2006
54216 TW10 1080   B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSTLpEQIGW Q5P Q244P OV observed variant Sequence This variant was found in 1/80 HLA-B*57/58 subjects, and in no HLA-B*57/5801 negative subjects infected with Clade B HIV-1. Martinez-Picado2006
54216 TW10 1081   B, C B, C Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQIGW T3N T242N E, R, RCR escape documented in this paper, reversion, replicative capacity reduced   This T242N variant from Clade B consensus was found in 24/80 HLA-B*57/5801 subjects, but only in 1/107 HLA-B*57/5801 negative subject infected with Clade B HIV-1. T242N from Clade C consensus was found in 68/126 HLA-B*57/5801 subjects, but only in 2/132 HLA-B*57/5801 negative subjects infected with Clade C HIV-1. It was thought to revert quickly to TSTLQEQIAW in HLA-B*57/5801 negative subjects since viral replication is affected in these mutants. Amino acid T at position Gag242 is the helix stabilizing residue in p24 Gag. Martinez-Picado2006
52759   1291 B     Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGN TSnLQEQIGN T3N T242N OV observed variant Sequence This variant is seen in 4/10 nonprogressors, 4/12 untreated progressors and 3/5 treated progressors. Migueles2003
52759   1292 B     Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGN TtnLQEQIaN S2T, T3N, G9A S241T, T242N, G248A OV observed variant Sequence This variant is seen in 1/12 untreated progressors. Migueles2003
52759   1293 B     Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGN TSnLQEQIaN T3N, G9A T242N, G248A OV observed variant Sequence This variant is seen in 2/10 nonprogressors, 5/12 untreated progressors and 2/5 treated progressors. Migueles2003
52759   1294 B     Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGN TSnLQEQvaN T3N, I8V, G9A T242N, I247V, G248A OV observed variant Sequence This variant is seen in 1/12 untreated progressor. Migueles2003
52759   1295 B     Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGN TSnLQEQIqN T3N, G9Q T242N, G248Q OV observed variant Sequence This variant is seen in 1/12 untreated progressor. Migueles2003
53833   1415 C     Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSTLQEQItW A9T A248T OV observed variant Sequence This variant was the autologous form seen in this non-HLA-B57 carrying mother, M5. The variant was transmitted to her infant, I5. Pillay2005
53833   1416 C     Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TSnLQEQIAW T3N T242N E escape documented in this paper CD8 T-cell Elispot - IFNy, Sequence This variant was a dominant, escape form (complete abrogation of response) that arose by week 33 in infant I5 who carried the restricting HLA allele, B57. Pillay2005
56143   1526 C     Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSnLQEQIGW T3N T242N CE calculated escape CD8 T-cell Elispot - IFNy, Sequence This variant is associated with lower viral loads, suggesting a fitness cost to the mutation. Rousseau2008
56143   1527 C     Gag 240 249 p24(108-117) 1507..1536 B57, B*5801 TSTLQEQIGW TSsLQEQIGW T3S T242S CE calculated escape CD8 T-cell Elispot - IFNy, Sequence This variant is associated with lower viral loads, suggesting a fitness cost to the mutation. Rousseau2008
55104 TW10 1645 B     Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSnLQEQIGW T3N T242N LE literature escape Previously reported in the literature This TW10 immunodominant epitope is an early CTL response target in HLA-B57+ LTNPs. After the acute phase of infection most subjects developed this escape variant which rapidly reverted to index sequence if transmitted to an HLA-B57- individual. Streeck2007a
56633 TW10 1987       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQVGW TSTLQEQiGW V8I V247I OV observed variant CD8 T-cell Elispot - IFNy, Intracellular cytokine staining, Sequence In patient 77 at day 159, the transmitted epitope disappeared and was substituted by two variants, TSTLQEQiGW (89%) and TSTLQEQVeW (11%). At the same time, response was high. Goonetilleke2009
56633 TW10 1988       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQVGW TSTLQEQVeW G9E G248E OV observed variant CD8 T-cell Elispot - IFNy, Intracellular cytokine staining, Sequence In patient 77 at day 159, the transmitted epitope disappeared and was substituted by two variants, TSTLQEQiGW (89%) and TSTLQEQVeW (11%). At the same time, response was high. Goonetilleke2009
56673   2128       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGW TnTLQEQIGW S2N S241N OV observed variant CD8 T-cell Elispot - IFNy, Intracellular cytokine staining, Sequence Patient CH58 carried this mutant. By day 85, two mutants, TnTLQEQIGW (22%) and TSTLQEQIeW (67%) dominated; pooled mutants were reactive to the same extent as the transmitted form. Goonetilleke2009
56673   2129       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGW TSTLQEQIeW G9E G248E OV observed variant CD8 T-cell Elispot - IFNy, Intracellular cytokine staining, Sequence Patient CH58 carried this mutant. By day 85, two mutants, TnTLQEQIGW (22%) and TSTLQEQIeW (67%) dominated; pooled mutants were reactive to the same extent as the transmitted form. Goonetilleke2009
57353 TW10 2225 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQIGW T3N T242N E, LE escape documented in this paper, literature escape CD8 T-cell Elispot - IFNy, Sequence This mutation TSnLQEQIGW, is the dominant, earliest mutation found in the sample group. It is present in lower, though not statistically significant, numbers in EC as compared to viremic subjects (CP, chronic progressors and VC, viremic controllers). It confers a fitness cost, and WT virus out competes it in culture. Compensatory mutations, H219Q, I223V and M228I are seen, correlating with increase in plasma VL (viral load). Miura2009a
57353 TW10 2226 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 {H...}TSTLQEQIGW {q...}TSnLQEQIGW H-21Q, T3N H219Q, T242N CM compensatory mutation CD8 T-cell Elispot - IFNy, Sequence H219Q, compensatory mutation to T242N is seen in greater numbers in subjects with increasing plasma VL. This compensatory mutation alone cannot account for VL differences between HLA-B57/B*5801-positive persons. Miura2009a
57353 TW10 2228 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 {M...}TSTLQEQIGW {i...}TSnLQEQIGW M-12I, T3N M228I, T242N CM compensatory mutation CD8 T-cell Elispot - IFNy, Sequence M228I, compensatory mutation to T242N, is seen in increasing numbers in subjects with increasing plasma VL. This compensatory mutation alone cannot account for VL differences between HLA-B57/B*5801-positive persons. Miura2009a
57353 TW10 2253 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{MTN} TSTLQEQIdW{MTh} N+3H, G9D N252H, G248D CM, RCR, SF compensatory mutation, replicative capacity reduced, susceptible form CD8 T-cell Elispot - IFNy, Relative replication capacity assay, Sequence This G248D rare mutation was seen in only 2 EC and 2 VC B*57/B*5801 + subjects in this cohort, and 1 non-HLA B*57/B*5801 subject from a different Canadian cohort. It was associated with mutations at N252H/R. Author protein location for these double mutants is G248D/N252H. The mutation most likely did not arise from a common ancestor but through in vivo selection after transmission. This double mutant had 54% VRC (viral replicative capacity) of the wild type NL4-3. Since the single mutant TSTLQEQIdW (not seen in vivo) has 24% VRC in vitro, the authors suggest the 252H variation is a compensatory mutation. The double mutation is never linked in vivo with T242N, but in vitro it is severely defective. Authors suggest the G248D and T242N pathways of escape are mutually exclusive and incompatible in vivo. The double mutant also affects VL by CTL response which is stronger than response to the wild type in subjects with autologous double mutant sequence. Miura2009a
57353 TW10 2254 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{MTN} TSTLQEQIdW{MTr} N+3R, G9D N252R, G248D CM, RCR, SF compensatory mutation, replicative capacity reduced, susceptible form CD8 T-cell Elispot - IFNy, Relative replication capacity assay This G248D rare mutation was seen in only 2 EC and 2 VC B*57/B*5801 + subjects in this cohort, and 1 non-HLA B*57/B*5801 subject from a different Canadian cohort. It was associated with mutations at N252H/R. Author protein location for these double mutants is G248D/N252R. The mutation most likely did not arise from a common ancestor but through in vivo selection after transmission. This double mutant had 74% VRC (viral replicative capacity) of the wild type NL4-3. Since the single mutant TSTLQEQIdW (not seen in vivo) has 24% VRC in vitro, the authors suggest the 252R variation is a compensatory mutation. The double mutation is never linked in vivo with T242N, but in vitro it is severely defective. Authors suggest the G248D and T242N pathways of escape are mutually exclusive and incompatible in vivo. The double mutant also affects VL by CTL response which is stronger than response to the wild type in subjects with autologous double mutant sequence. Miura2009a
52918 TW10 2284 C     Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIAW TS*LQEQIAW T3* T242* OV observed variant   174 people who have C clade infections were studied -- those who carried B57 have 2 positions in which their HIV Gag consensus is different than the C consensus. One mutation is within this epitope, TW10, at position 3, and is believed to be a TCR contact residue. The mutation is not specified in the study. Draenert2004a
56633 TW10 2332       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQVGW TSnLQEQiaW T3N, V8I, G9A T242N, V247I, G248A IE inferred escape CD8 T-cell Elispot - IFNy, Intracellular cytokine staining In patient CH77 at 592 days, this variant predominated and the authors infer escape. Goonetilleke2009
57379 TW10 wt 2339       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGW TSTLQEQIaW G9A G248A LE literature escape Tetramer binding Natural variant TSTLQEQIaW had no change in binding over wild type TW10 to inhibitory receptor ILT4 on CD14+ monocytes. Yang2010
57382 TW10 2343 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQEQIaW G9A G248A OV observed variant   One HLA-B*5703 positive patient with low viral load carried this mutation at enrollment. Durand2010
57382 TW10 2344 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQdQvaW E6D, I8V, G9A E245D, I247V, G248A OV observed variant Sequence One HLA-B*5701 positive patient with low viral load carried this mutation at enrollment. Durand2010
57382 TW10 2345 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A OV observed variant Sequence One HLA-B*5703 positive patient with low viral load carried this mutation by month 6; one HLA-B*5701 positive patient with low viral load carried it by month 28. Durand2010
57382 TW10 2346 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQEQItW G9T G248T OV observed variant Sequence One HLA-B*5703 positive patient with low viral load carried this mutation at enrollment. Durand2010
57382 TW10 2347 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQEQIeW G9E G248E OV observed variant Sequence One HLA-B*5702 positive patient with low viral load carried this mutation at enrollment. Durand2010
57382 TW10 2348 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLeEQIdW Q5E, G9D Q244E, G248D OV observed variant Sequence One HLA-B*5702 positive patient with low viral load carried this mutation at month 13 after enrollment. Durand2010
57382 TW10 2349 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLQEQvaW T3N, I8V, G9A T242N, I247V, G248A OV observed variant Sequence One HLA-B*5701 positive patient with low viral load carried this variant from month 10 onwards. Durand2010
57382 TW10 2350 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQEQIdW G9D G248D OV observed variant Sequence One HLA-B*5702 positive patient with low viral load carried this mutation a month after enrollment; one HLA-B*5701 positive patient with increased viral load also carried this variant from enrollment on. Durand2010
57382 TW10 2351 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQEQInW G9N G248N OV observed variant Sequence One HLA-B*5703 positive patient with increased viral load carried this mutation at enrollment. Durand2010
57382 TW10 2352 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLQEQInW T3N, G9N T242N, G248N OV observed variant Sequence One HLA-B*5703 positive patient carried this mutation from enrollment on. Durand2010
57418 TW10 2368 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLQEQIGW T3N T242N LE literature escape Sequence The T242N mutation in p24-Gag was seen in all subjects except for one controller, CH-13. Controllers CH-04 and CH-03 who carried this particular variant, TSnLQEQIGW, did not carry any compensatory mutations known. Tang2010
57418 TW10 2369 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLQEQIqW T3N, G9Q T242N, G248Q CM, LE compensatory mutation, literature escape Sequence This T242N carrying variant, TSnLQEQIqW, is accompanied by compensatory mutations H219Q and M228I (but not I223V) in progressor CH-12. Tang2010
57418 TW10 2370 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A CM, LE compensatory mutation, literature escape Sequence This T242N mutation carrying variant, TSnLQEQIaW, was accompanied by compensatory mutations H219Q and M228I (but not I223V) in progressor CH-01. In controller CH-22, however, this same variant of TW10 was not accompanied by an compensatory mutations studied. Tang2010
57418 TW10 2371 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQEQIdW G9D G248D LE literature escape Sequence This rare mutant, TSTLQEQIdW, found only in controller CH-13, did not carry the usual T242N mutation and likely represents an alternative escape pathway from epitope TW10. Tang2010
57418 TW10 2372 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLQEQItW T3N, G9T T242N, G248T CM, LE compensatory mutation, literature escape Sequence This T242N carrying variant, TSnLQEQItW, is accompanied by compensatory mutations H219Q, I223V and M228I in subject CH-08. Tang2010
57418 TW10 2373 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLaEQIaW T3N, Q5A, G9A T242N, Q244A, G248A CM, LE compensatory mutation, literature escape Sequence This T242N carrying variant, TSnLaEQIaW, was accompanied by compensatory mutations H219Q, I223V and M228L in progressor CH-11. Tang2010
57555   2527 B B B Gag 240 249 p24(108-117) 1507..1536   TSTLQEQIGW TSnLQEQIGW T3N T242N E escape documented in this paper CD4 T-cell Elispot - IFNy The variant TSnLQEQIGW evolved to dominate the quasispecies, and was not recognized compared to the index peptide TSTLQEQIGW by the PBMC from time points around the time of response decline, indicating escape. Turnbull2009
57261 TW10 2548 A1 A1 A1 Gag 240 249 p24(108-117) 1507..1536 B*57 TSTPQEQIGW TSTPtEQIGW Q5T Q244T NSF non-susceptible form CD8 T-cell Elispot - IFNy The majority of A1-infected B*57+ subjects who responded to TW10 did not respond to P243T TSTPtEQIGW or I247L TSTPQEQlGW variants, supporting previous findings that these represent escape mutations in clade A1. McKinnon2009
57261 TW10 2549 A1 A1 A1 Gag 240 249 p24(108-117) 1507..1536 B*57 TSTPQEQIGW TSTPQEQlGW I8L I247L NSF non-susceptible form CD8 T-cell Elispot - IFNy The majority of A1-infected B*57+ subjects who responded to TW10 did not respond to P243T TSTPtEQIGW or I247L TSTPQEQlGW variants, supporting previous findings that these represent escape mutations in clade A1. McKinnon2009
57261 TW10 2550 A1 A1 B, D Gag 240 249 p24(108-117) 1507..1536 B*57 TSTPQEQIGW TSTlQEQIGW P4L P243L DR diminished response CD8 T-cell Elispot - IFNy In clade A1-infected patients the recognition of the B/D consensus TSTlQEQIGW was diminished compared to that of clade A1 TSTPQEQIGW. The mutant T242N TSnlQEQIGW was previously documented for clades B and D as escape. However, despite the presumed absence of this variant in these subjects' autologous sequences, the clade B/D escape variant TSnlQEQIGW was recognized at a magnitude similar to that of consensus clade A1 TSTPQEQIGW. McKinnon2009
57261 TW10 2551 A1 A1 B, D Gag 240 249 p24(108-117) 1507..1536 B*57 TSTPQEQIGW TSnlQEQIGW T3N, P4L T242N, P243L SF susceptible form CD8 T-cell Elispot - IFNy In clade A1-infected patients the recognition of the B/D consensus TSTlQEQIGW was diminished compared to that of clade A1 TSTPQEQIGW. The mutant T242N TSnlQEQIGW was previously documented for clades B and D as escape. However, despite the presumed absence of this variant in these subjects' autologous sequences, the clade B/D escape variant TSnlQEQIGW was recognized at a magnitude similar to that of consensus clade A1 TSTPQEQIGW. McKinnon2009
57648 TW10 2566       Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSnLQEQIGW T3N T242N E escape documented in this paper Relative replication capacity assay Of 2 HLA-B57-positive early controllers both had, at the earliest time point tested, signature B57 mutations in Gag that impaired viral replication capacity: T242N in TSTLQEQIGW (TSnLQEQIGW) and I147L in ISPRTLNAW (lSPRTLNAW). Miura2010
57846 TW10 2649 B B B Gag 240 249 p24(108-117) 1507..1536 B*5703 TSTLQEQIGW TSTLQEQIeW G9E G248E E, SF escape documented in this paper, susceptible form CD8 T-cell Elispot - IFNy, Longitudinal study Variant arose during early infection in 2 B*57-positive patients. The variant failed to evade TW10-specific T cells, but severely reduced interaction between KIR3DL1 and HLA-B*5703. Brackenridge2011
57846 TW10 2650 B B B Gag 240 249 p24(108-117) 1507..1536 B*5703 TSTLQEQIGW TSnLQEQIGW T3N T242N E escape documented in this paper CD8 T-cell Elispot - IFNy, Longitudinal study Variant arose during early infection in 2 B*57-positive patients, but disappeared by day 350. The T3N change abrogated T cell recognition of the TW10 epitope, but was not associated with loss of KIR binding to HLA-B*57. Brackenridge2011
57676   2672 B A, B, C, D B, D Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSnLQEQIGW T3N T242N SF, SSF susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Intracellular cytokine staining Variant TSnLQEQIGW was found at a frequency of 3 and 5 in clades B and D respectively. Koup2010
57676   2673 B A, B, C, D A, B, C, D Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSTLQEQIaW G9A G248A SF, SSF susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Intracellular cytokine staining Variant TSTLQEQIaW was found at frequencies of 5, 8, 63 and 36 in clades A, B, C and D respectively. Koup2010
57676   2674 B A, B, C, D A, B, C, D Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSTpQEQIGW L4P L243P SF, SSF susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Intracellular cytokine staining Variant TSTpQEQIGW was found at a frequency of 42 in clade A. Koup2010
58008 TW10 2696 B B B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSnLQEQIGW T3N T242N LE, P literature escape, processing   B57-TW10 was selected for analysis based on having known early mutants (T3N and T3N-G9A or T3N-G9D) that were predicted to have reduced intracellular stability. Mutant T3N was stable, while T3N-G9A or T3N-G9D severely reduced half-life. Single mutants G9A and G9D also displayed decreased half-lives. Lazaro2011
58008 TW10 2697 B B B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A LE, P literature escape, processing   B57-TW10 was selected for analysis based on having known early mutants (T3N and T3N-G9A or T3N-G9D) that were predicted to have reduced intracellular stability. Mutant T3N was stable, while T3N-G9A or T3N-G9D severely reduced half-life. Single mutants G9A and G9D also displayed decreased half-lives. Lazaro2011
58008 TW10 2698 B B B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSnLQEQIdW T3N, G9D T242N, G248D LE, P literature escape, processing   B57-TW10 was selected for analysis based on having known early mutants (T3N and T3N-G9A or T3N-G9D) that were predicted to have reduced intracellular stability. Mutant T3N was stable, while T3N-G9A or T3N-G9D severely reduced half-life. Single mutants G9A and G9D also displayed decreased half-lives. Lazaro2011
58008 TW10 2699 B B B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSTLQEQIaW G9A G248A A, P HLA association, processing   B57-TW10 was selected for analysis based on having known early mutants (T3N and T3N-G9A or T3N-G9D) that were predicted to have reduced intracellular stability. Mutant T3N was stable, while T3N-G9A or T3N-G9D severely reduced half-life. Single mutants G9A and G9D also displayed decreased half-lives. Lazaro2011
58008 TW10 2700 B B B Gag 240 249 p24(108-117) 1507..1536 B57 TSTLQEQIGW TSTLQEQIdW G9D G248D A, P HLA association, processing   B57-TW10 was selected for analysis based on having known early mutants (T3N and T3N-G9A or T3N-G9D) that were predicted to have reduced intracellular stability. Mutant T3N was stable, while T3N-G9A or T3N-G9D severely reduced half-life. Single mutants G9A and G9D also displayed decreased half-lives. Lazaro2011
57873 TW10 2714 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSTLpEQIAW Q5P Q244P ? unclear Sequence 4/18 and 4/12 sampled viral sequences in subject CAP217 carried this variant, TSTLpEQIAW, 3.4 and 3.8 months post infection. Chopera2011
57873 TW10 2715 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSTLQEeIAW Q7E Q246E ? unclear Sequence 1/18 sampled viral sequences in subject CAP217 carried this variant, TSTLQEeIAW, 3.4 months post infection. Chopera2011
57873 TW10 2716 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSTLQEQIAW|i M+1I M250I OV, SF observed variant, susceptible form CD8 T-cell Elispot - IFNy, Sequence All sampled viral sequences in subject CAP268 carried this flanking mutation, TSTLQEQIAW|i, 1.8, 5.5, 12.3, 19.8 and 31.4 months post infection. While this subject responded to TW10, not surprisingly no epitopic escapes were found as the M250I mutation here has been previously associated with reduced frequency of escape in TW10. Chopera2011
57873 TW10 2717 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSTLQEQItW A9T A248T ? unclear Sequence 2/10 sampled viral sequences in subject CAP229 carried this variant, TSTLQEQItW, 1.8 months post infection. Chopera2011
57873 TW10 2718 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSnLQEQItW T3N, A9T T242N, A248T OV, SF observed variant, susceptible form CD8 T-cell Elispot - IFNy, Sequence 2/10, 6/6, 3/3, 23/23, 15/15, 24/24, 15/15 and 16/16 sampled viral sequences in subject CAP229 carried this variant, TSTLQEQItW, 1.8, 2.1, 4.8, 5.8, 18.4, 21.2, 24.2 and 28.1 months post infection. At 2.1 months post-infection, CTL response was reduced. Chopera2011
57873 TW10 2719 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSnLQEQvAW T3N, I8V T242N, I247V OV, SF observed variant, susceptible form CD8 T-cell Elispot - IFNy, Sequence 9/9 and 9/9 sampled viral sequences in subject CAP239 carried this variant, TSnLQEQvAW, 5.1 and 18.2 months post infection. At 5.1 months post-infection, CTL response was reduced. Chopera2011
57873 TW10 2720 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSTLQEQvAW I8V I247V OV observed variant Sequence 20/21 sampled viral sequences in subject CAP239 carried this variant, TSTLQEQvAW, 0.5 months post infection. Chopera2011
57873 TW10 2721 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSTiQEQvtW L4I, I8V, A9T L243I, I247V, A248T ? unclear Sequence 1/21 sampled viral sequences in subject CAP239 carried this variant, TSTiQEQvtW, 0.5 months post infection. Chopera2011
57873 TW10 2722 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSnLQEQvtW T3N, I8V, A9T T242N, I247V, A248T SF susceptible form CD8 T-cell Elispot - IFNy, Sequence 27/27 and 19/19 sampled viral sequences in subject CAP239 carried this variant, TSnLQEQvtW, 1.2 and 1.4 months post infection and CTL response when tested, was reduced. Chopera2011
57873 TW10 2723 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSTLhEQvqW Q5H, I8V, A9Q Q244H, I247V, A248Q NSF non-susceptible form CD8 T-cell Elispot - IFNy, Sequence 2/9 sampled viral sequences in subject CAP274 carried this variant, TSTLhEQvqW, 2.4 months post infection. Chopera2011
57873 TW10 2724 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSnLQEQvqW T3N, I8V, A9Q T242N, I247V, A248Q NSF non-susceptible form CD8 T-cell Elispot - IFNy, Sequence All viral sequences sampled in subject CAP274 carried this variant, TSnLQEQvqW, 2.4, 5.1 and 13.9 months post infection. Chopera2011
57873 TW10 2725 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSTLtEQIAW Q5T Q244T ? unclear Sequence 1/9 sampled viral sequences in subject CAP217 carried this variant, TSTLtEQIAW, 5.2 months post infection. Chopera2011
57873 TW10 2726 C C C Gag 240 249 p24(108-117) 1507..1536 B*5801 TSTLQEQIAW TSnLQEQIAW T3N T242N ?, OV, SF unclear, observed variant, susceptible form CD8 T-cell Elispot - IFNy, Sequence This variant at position 3, TSnLQEQIAW, was seen in subject CAP217. 6/12, 12/12, 7/9, 10/10 and 14/14 sequences carried the variant at 3.8, 4.3, 5.2, 6.2 and 13.8 months post-infection. At 4.3 months post-infection, CTL response was reduced. Chopera2011
58229   2796 B B B Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGW TSnLQEQIGW T3N T242N IE inferred escape Sequence 1/9, 2/9, 1/2 and 3/3 sequences of epitope TSTLQEQIGW varied at 45, 85, 154 and 350 DFOSx to TSnLQEQIGW. Position 110 in the epitope is marked as being under selection to vary. Ferrari2011
58229   2798 B B B Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGW TSTLQEQIeW G9E G248E IE inferred escape Sequence 1/2, 6/9 and 1/2 sequences of epitope TSTLQEQIGW varied at 45, 85 and 154 DFOSx to TSTLQEQIeW. Position 116 in the epitope is marked as being under selection to vary. Ferrari2011
58236   2806 B B B Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQVGW TSTLQEQiGW V8I V247I IE inferred escape Sequence 8/9 sequences of epitope TSTLQEQVGW varied at 159 DFOSx to ITSTLQEQiGW. Position 115 in the peptide is marked as being under selection to vary. Ferrari2011
58236   2808 B B B Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQVGW TSTLQEQVeW G9E G248E OV observed variant Sequence 1/9 sequences of epitope TSTLQEQVGW varied at 159 DFOSx to TSTLQEQVeW. Position 116 in the peptide is marked as being under selection to vary. Ferrari2011
58236   2809 B B B Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQVGW TSnLQEQiaW T3N, V8I, G9A T242N, V247I, G248A OV observed variant Sequence 8/8 sequences of epitope TSTLQEQVGW varied at 592 DFOSx to TSnLQEQiaW. Ferrari2011
57913   2827       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A E escape documented in this paper Tetramer binding   Fadda2011
57913   2829       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A E escape documented in this paper Tetramer binding   Fadda2011
57913   2830       Gag 240 249 p24(108-117) 1507..1536 B*5701 TSTLQEQIGW TSTLQEQIdW G9D G248D E escape documented in this paper Tetramer binding   Fadda2011
58356 TW10 2890 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLtEQvaW Q5T, I8V, G9A Q244T, I247V, G248A DR diminished response CD8 T-cell Elispot - IFNy, CTL suppression of replication Variant TSTLtEQvaW elicited a highly diminished CTL response and when present in a virus, greatly reduced its replicative capacity. OConnell2011
58356 TW10 2891 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLaEQvaW Q5A, I8V, G9A Q244A, I247V, G248A DR diminished response CD8 T-cell Elispot - IFNy, CTL suppression of replication Variant TSTLaEQvaW elicited a highly diminished CTL response and when present in virus, greatly reduced its replicative capacity. OConnell2011
58356 TW10 2892 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLsEQvaW Q5S, I8V, G9A Q244S, I247V, G248A DR diminished response CD8 T-cell Elispot - IFNy, CTL suppression of replication Variant TSTLsEQvaW elicited a highly diminished CTL response and when present in virus, greatly reduced its replicative capacity. OConnell2011
58356 TW10 2893 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLsEQIaW Q5S, G9A Q244S, G248A DR diminished response CD8 T-cell Elispot - IFNy, CTL suppression of replication Variant TSTLsEQIaW elicited a highly diminished CTL response and when present in virus, greatly reduced its replicative capacity. OConnell2011
58356 TW10 2894 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLvEQIaW Q5V, G9A Q244V, G248A DR diminished response CD8 T-cell Elispot - IFNy, CTL suppression of replication Variant TSTLvEQIaW elicited a highly diminished CTL response and when present in virus, greatly reduced its replicative capacity. OConnell2011
58356 TW10 2895 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLtEQIaW Q5T, G9A Q244T, G248A DR diminished response CD8 T-cell Elispot - IFNy, CTL suppression of replication Variant TSTLtEQIaW elicited a highly diminished CTL response and when present in virus, greatly reduced its replicative capacity. OConnell2011
58356 TW10 2896 B B B Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLaEQIaW Q5A, G9A Q244A, G248A DR diminished response CD8 T-cell Elispot - IFNy, CTL suppression of replication Variant TSTLaEQIaW elicited a highly diminished CTL response and when present in virus, greatly reduced its replicative capacity. OConnell2011
57353 TW10 2996 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 {I...}TSTLQEQIGW {v...}TSnLQEQIGW I-17V, T3N I223V, T242N CM compensatory mutation Sequence I223V, compensatory mutation to T242N, is seen in increasing numbers in subjects with increasing plasma VL. This compensatory mutation alone cannot account for VL differences between HLA-B57/B*5801-positive persons. Miura2009a
57353 TW10 2999 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{M} TSTLQEQmtW{i} M+1I, I8M, G9T M250I, I247M, G248T RCR replicative capacity reduced CD8 T-cell Elispot - IFNy, Relative replication capacity assay, Sequence Variant TSTLQEQmtW{i} (author designation I247M/G248T/M250I/252N) displayed a lower replication capacity than variant G248D (TSTLQEQIdW) and was found in one elite controller. Miura2009a
57353 TW10 3000 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{MTN} TSTLQEQmaW{iTh} M+1I, N+3H, I8M, G9A M250I, N252H, I247M, G248A CM, RCR compensatory mutation, replicative capacity reduced CD8 T-cell Elispot - IFNy, Relative replication capacity assay, Sequence Variant TSTLQEQmaW{iTh} (author designation I247M/G248A/M250I/N252H) was found in 2 elite controllers. It displayed an improved replication capacity (VRC) over variant TSTLQEQmaW{iTN}, but had a slightly lower VRC (91%) than wild type virus, supporting the compensatory effect of N252H mutation. Miura2009a
57353 TW10 3001 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{M} TSTLQEQmaW{i} M+1I, I8M, G9A M250I, I247M, G248A E, RCR escape documented in this paper, replicative capacity reduced CD8 T-cell Elispot - IFNy, Relative replication capacity assay, Sequence Variant TSTLQEQmaW{i} (author designation I247M/G248A/M250I/252N) displayed a reduced replication capacity at 71% of wild type virus. It was found in one elite controller, BEC33, who also carried 3 other rare variants. Thus the M250I mutation likely induces a considerable fitness defect, while the I247M/G248A mutations are escapes [see variant TSTLQEQmaW]. Miura2009a
57353 TW10 3002 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{M} TSTLQEQmaW{v} M+1V, I8M, G9A M250V, I247M, G248A E, RCR escape documented in this paper, replicative capacity reduced CD8 T-cell Elispot - IFNy, Relative replication capacity assay, Sequence Variant TSTLQEQmaW{v} (author designation I247M/G248A/M250V/252N) was extremely attenuated, producing almost no live virus. It was found in one elite controller, BEC33, who also carried 3 other rare variants. The variant peptide was also not able to elicit CTL response. Miura2009a
57353 TW10 3003 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{M} TSTLQEQIaW{i} M+1I, G9A M250I, G248A RCR, SF replicative capacity reduced, susceptible form CD8 T-cell Elispot - IFNy, Relative replication capacity assay, Sequence Variant TSTLQEQIaW{i} (author designation G248A/M250I/252N) displayed a reduced replication capacity at 62% of wild type virus'. This peptide was able to elicit a CTL response. It was found in one elite controller, BEC33, who also carried 3 other rare variants. Miura2009a
57353 TW10 3004 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{MTN} TSTLQEQlnW{iTN} M+1I, I8L, G9N M250I, I247L, G248N ?, RCR unclear, replicative capacity reduced Relative replication capacity assay, Sequence Variant TSTLQEQlnW|iTN (author designation I247L/G248N/M250I/252N) displayed reduced viral replication at 79% of wild type. Peptide TSTLQEQlnW elicited CTL response greater than that of TW10. Miura2009a
57353 TW10 3006 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{M} TSnLQEQIaW{i} M+1I, T3N, G9A M250I, T242N, G248A RCR replicative capacity reduced CD8 T-cell Elispot - IFNy, Relative replication capacity assay, Sequence Variant TSnLQEQIaW{i} (author designation T242N/G248A/M250I/252N) was extremely attenuated, producing no live virus. Miura2009a
57353 TW10 3007 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSTLQEQIaW G9A G248A SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant TSTLQEQIaW (author designation G248A) elicited a stronger CTL response in a controlling subject than wild type TW10 did. It was an autologous sequence in this patient. Miura2009a
57353 TW10 3008 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSTLQEQmaW I8M, G9A I247M, G248A E, RCR escape documented in this paper, replicative capacity reduced CD8 T-cell Elispot - IFNy, Relative replication capacity assay, Sequence Variant peptide TSTLQEQmaW (author designation I247M/G248A/252N) was unable to elicit CTL response in one subject, suggesting they represent mutations leading to escape. This peptide elicited low response, less than to WT TW10, when it was the autologous sequence in another subject. The variant virus showed reduced viral replication. Miura2009a
57353 TW10 3009 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSTLQEQlnW I8L, G9N I247L, G248N SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant peptide TSTLQEQlnW (author designation I247L/G248N) elicited CTL response greater than that of TW10 in a controller where it was the autologous sequence. When combined with a downstream mutation at M250I, however (author designation I247L/G248N/M250I/252N), variant TSTLQEQlnW|iTN has a reduced viral replication capacity. Miura2009a
57353 TW10 3010 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{M} TSnLQEQlnW{i} M+1I, T3N, I8L, G9N M250I, T242N, I247L, G248N RCR replicative capacity reduced Relative replication capacity assay, Sequence Variant TSnLQEQlnW{i} (author designation T242N/I247L/G248N/M250I/252N) displayed defective viral replication resulting in insufficient titers to obtain virus for tests. Miura2009a
57353 TW10 3011 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{M} TSnLQEQInW{i} M+1I, T3N, G9N M250I, T242N, G248N RCR replicative capacity reduced Relative replication capacity assay, Sequence Variant TSnLQEQInW{i} (author designation T242N/G248N/M250I/252N) displayed defective viral replication resulting in insufficient titers to obtain virus for tests. Miura2009a
57353 TW10 3013 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{MTN} TSnLQEQInW{MTg} T3N, N+3G, G9N T242N, N252G, G248N RCR replicative capacity reduced Relative replication capacity assay, Sequence Variant TSnLQEQInW{MTg} (author designation T242N/G248N/N252G) displayed reduced replication capacity, 85% of wild type virus. Miura2009a
57353 TW10 3015 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{MTN} TSTLQEQInW{MTg} N+3G, G9N N252G, G248N RCR replicative capacity reduced Relative replication capacity assay, Sequence Variant TSnLQEQInW{MTg} (author designation G248N/N252G) displayed slightly reduced replication capacity, 89% of wild type virus. Miura2009a
57353 TW10 3016 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{MTN} TSnLQEQIGW{MTg} T3N, N+3G T242N, N252G RCR replicative capacity reduced Relative replication capacity assay, Sequence Variant TSnLQEQIGW{MTg} (author designation N252G) displayed slightly reduced replication capacity, 72% of wild type virus. Miura2009a
57353 TW10 3017 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQItW T3N, G9T T242N, G248T NSF, RCR, SF non-susceptible form, replicative capacity reduced, susceptible form Relative replication capacity assay, Sequence Variant TSnLQEQItW (author designation T242N/G248N) displayed very slightly reduced replication capacity at 92% of wild type virus. The subject carrying this autologous virus was able to recognize the variant peptide even more strongly than wild type TW10. All subjects tested who recognized the T242N variant of TW10, whether they were controllers or not, were also able to recognize variant peptides of the T242N/G248X pattern (including this peptide, TSnLQEQItW). The variant, however, was not recognized by any subject where it was a non-autologous sequence. Miura2009a
57353 TW10 3018 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQItr W10R, T3N, G9T W249R, T242N, G248T E escape documented in this paper Relative replication capacity assay Variant TSnLQEQItr [author designation T242N/G248T/W249R] was found in only 1 viremic controller subject. An in vitro synthesized mutant proviral NL4-3 was unable to generate enough virus for experimentation. Position 249 is the anchor position of TW10. Miura2009a
57353 TW10 3019 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQIaW T3N, G9A T242N, G248A E escape documented in this paper CD8 T-cell Elispot - IFNy, Sequence Variant peptide TSnLQEQIaW was not able to elicit CTL response in 7/8 subjects queried. One subject elicited low IFN-γ at higher peptide concentrations. Miura2009a
57353 TW10 3020 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSTLQEQIdW G9D G248D NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant peptide TSTLQEQIdW elicited CTL response in 6/8 controllers queried, where 4 of the subjects carried it as an autologous sequence. The 2 non-responders did not carry this variant as autologous. Miura2009a
57353 TW10 3021 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW TSnLQEQInW T3N, G9N T242N, G248N NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant peptide TSnLQEQInW elicited low CTL response, and in only 1/8 controllers queried in whom it was the autologous sequence. Miura2009a
58688 TW10 3102 C C C Gag 240 249 p24(108-117) 1507..1536 B*5702, B*5703, B*5801 TSTLQEQIAW TSxLQEQIAW T3X T242X OV observed variant Sequence Mutation TSxLQEQIAW was seen in >75% of both HLA-B*5703 and -B*5702 positive subjects, and in just under 75% of HLA-B*5801 carrying subjects. Kloverpris2012
58688 TW10 3103 C C C Gag 240 249 p24(108-117) 1507..1536 B*5702, B*5703, B*5801 TSTLQEQIAW TSTLQEQxAW I8X I247X OV observed variant Sequence Mutation TSTLQEQxAW was seen in ˜25% of HLA-B*5703-positive subjects, and in very few HLA-B*5801 or -B*5702 carrying subjects. Kloverpris2012
58744   3132       Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQEQIaW G9A G248A SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Mutant TSTLQEQIaW was seen in and recognized by subject ES38. Buckheit2012
58744   3133       Gag 240 249 p24(108-117) 1507..1536 B*57 TSTLQEQIGW TSTLQEQvaW I8V, G9A I247V, G248A NSF non-susceptible form CD8 T-cell Elispot - IFNy, Sequence Mutant TSTLQEQvaW was seen in CP2 Gag sequences even though CP2 does not carry the HLA-B*57 allele. Subject CP2 was not able to recognize this sequence by EliSpot. Buckheit2012
58777 TW10 3142 B, C B, C B, C Gag 240 249 p24(108-117) 1507..1536   TSTLQEQIAW{M} TSTLaEQIAW{i} M+1I, Q5A M250I, Q244A DR diminished response Relative replication capacity assay One of the subtype C variants. Chopera2012
58777 TW10 3143 B, C B, C C Gag 240 249 p24(108-117) 1507..1536   TSTLQEQIAW{M} TSTLQEQmAW{i} M+1I, I8M M250I, I247M DR diminished response Relative replication capacity assay One of the subtype C mutants. Chopera2012
58777 TW10 3144 B, C B, C B, C Gag 240 249 p24(108-117) 1507..1536   TSTLQEQIAW{M} TSTLQEQvAW{i} M+1I, Q5A M250I, Q244A DR diminished response Relative replication capacity assay TSTLQEQIAW{i} is the M250I mutation under study. Chopera2012
57353 TW10 3200 B B B Gag 240 249 p24(108-117) 1507..1536 B*57, B*5801 TSTLQEQIGW{M} TSTLQEQlnW{i} M+1I, I8L, G9N M250I, I247L, G248N ?, RCR unclear, replicative capacity reduced Relative replication capacity assay, Sequence Variant TSTLQEQlnW{i} (author designation I247L/G248N/M250I/252N) displayed reduced viral replication at 79% of wild type. Peptide TSTLQEQlnW elicited CTL response greater than that of TW10. Miura2009a
53676   333 B, D     Gag 241 249 p24(109-117) 1510..1536 B58 STLQEQIGW STLQEQIaW G8A G248A OV observed variant   Cross-clade T cell responses are frequently induced in individuals infected with different HIV-1 clades. There was an inverse correlation between the height of responses and epitope sequence divergence. For Gag epitopes, the magnitude of the response was directly linked to the homology between HLA anchor residues. Geels2005
56057 Gag242 202       Gag 242 250 p24(110-118) 1513..1539 A2 TLQEQIGWM sLQEQIGWM T1S T242S OV observed variant   One HLA-A2 patient did not respond to the TLQEQIGWM epitope but the variant peptide was observed in the patient. Fomsgaard2008
55368 Gag 242 1668       Gag 242 250 p24(110-118) 1513..1539 A2 TLQEQIGWM TLQEQIaWM G7A G248A OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subjects Pt15 and Pt33 carried this variant and were unable to recognize the challenge HXB2 form. Subjects Pt35 and Pt41 carried the HXB2 sequence and were able to recognize it; all others Pt16, Pt17, Pt18, Pt21, Pt23 and Pt35 did carry the HXB2 epitope, but could not recognize it. Thorn2007
55368 Gag 242 1669       Gag 242 250 p24(110-118) 1513..1539 A2 TLQEQIGWM nLQEQIGWM T1N T242N OV observed variant CD8 T-cell Elispot - IFNy, Flow cytometric T-cell cytokine assay, Sequence Subject Pt30 carried this variant and was unable to recognize the challenge HXB2 form, NTVATLYCV. Thorn2007
58747   3136       Gag 249 263 p24(117-131) 1534..1578   WMTNNPPIPVGEIYK WMTsNPPvPVGEIYK N4S, I8V N252S, I256V NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, CTL suppression of replication, Intracellular cytokine staining WMTsNPPvPVGEIYK was a variant found in both CP2 and ES38 HIV-1 sequences even though it was recognized by subject CP2 and not ES38. Buckheit2012
53072 Gag 271 1114 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTnNPPIPV S3N S252N SF susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV, induced CTL that were able to recognize variant peptide MTnNPPIPV; and mice immunized with subtype B epitope form MTnNPPIPV induced CTL that also recognized self peptide, MTnNPPIPV. McKinney2004
53072 Gag 271 1115 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTSNPPvPV I7V I256V SF susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV induced CTL that were able to recognize variant MTSNPPvPV; but mice immunized with subtype B form MTnNPPIPV induced CTL that were unable to recognize the same subtype C variant, MTSNPPvPV. McKinney2004
53072 Gag 271 1116 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTSdPPvPV N4D, I7V N253D, I256V SF susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV induced CTL that were able to recognize variant MTSdPPvPV; but mice immunized with subtype B form MTnNPPIPV induced CTL that were unable to recognize the same subtype C variant, MTSdPPvPV. McKinney2004
53072 Gag 271 1117 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTSNPaIPV P6A P255A DHB, NSF, SF diminished HLA binding or increased off-rate, non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV induced CTL that were able to recognize variant MTSNPaIPV; but mice immunized with subtype B form MTnNPPIPV induced CTL that were unable to recognize the same subtype C variant, MTSNPaIPV. Binding of variant MTSNPaIPV to HLA-A2 was extremely weak. McKinney2004
53072 Gag 271 1118 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTgNPPIPV S3G S252G SF susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV induced CTL that were able to recognize variant MTgNPPIPV; but mice immunized with subtype B form MTnNPPIPV induced CTL that were unable to recognize the same subtype C variant, MTgNPPIPV. McKinney2004
53072 Gag 271 1119 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTgNPsIPV S3G, P6S S252G, P255S NSF non-susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV, induced CTL that were unable to recognize variant MTgNPsIPV; and mice immunized with subtype B form MTnNPPIPV induced CTL that were also unable to recognize the same subtype C variant. McKinney2004
53072 Gag 271 1120 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTgNPaIPV S3G, P6A S252G, P255A NSF non-susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV, induced CTL that were unable to recognize variant MTgNPaIPV; and mice immunized with subtype B form MTnNPPIPV induced CTL that were also unable to recognize the same subtype C variant. McKinney2004
53072 Gag 271 1121 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTgNPPvPV S3G, I7V S252G, I256V DHB, NSF, SF diminished HLA binding or increased off-rate, non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV induced CTL that were able to recognize variant MTgNPPvPV; but mice immunized with subtype B form MTnNPPIPV, induced CTL that were unable to recognize the same subtype C variant, MTgNPPvPV. Binding of variant MTgNPPvPV to HLA-A2 was extremely weak. McKinney2004
53072 Gag 271 1122 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTaNPPIPV S3A S252A SF susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV induced CTL that were able to recognize variant MTaNPPIPV; but mice immunized with subtype B form MTnNPPIPV, induced CTL that were unable to recognize the same subtype C variant, MTaNPPIPV. McKinney2004
53072 Gag 271 1123 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MTaNPPvPV S3A, I7V S252A, I256V SF susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV induced CTL that were able to recognize variant MTaNPPvPV; but mice immunized with subtype B form MTnNPPIPV, induced CTL that were unable to recognize the same subtype C variant, MTaNPPvPV. McKinney2004
53072 Gag 271 1125 M B, C C Gag 250 258 p24(118-126) 1537..1563 A*0201 MTSNPPIPV MThNPPIPV S3H S252H SF susceptible form CD8 T-cell Elispot - IFNy, HLA binding Mice immunized with subtype C epitope MTSNPPIPV induced CTL that were able to recognize variant MThNPPIPV; but mice immunized with subtype B form MTnNPPIPV, induced CTL that were barely able to recognize the same subtype C variant, MThNPPIPV. McKinney2004
53842 MV9 1575       Gag 250 258 p24(118-126) 1537..1563 A2 MTNNPPIPV MThNPPIPV N3H N252H OV observed variant Sequence This variant from the HXB2 sequence was present in the non-HLA-A2 allele carrying mother, M-1004, as well as her restricting-HLA-A2-carrying infant, P-1115. This variant was still detected at 12 months of age in infant P-1115. Sanchez-Merino2005
58600 NY10, NY10-260D 3081 C C C Gag 253 262 p24(121-130) 1546..1575 B*3501 NPPIPVGDIY NPPIPVGeIY D8E D260E DHB, DR, E, SNSF diminished HLA binding or increased off-rate, diminished response, escape documented in this paper, subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy, HLA binding, Intracellular cytokine staining, Sequence, Tetramer binding The C clade variant, NPPIPVGeIY, is also the major B clade form of epitope NY10. This NY10-260E variant binds to HLA-B*3105 10x less well than the wt and is 3x less stable. Matthews2012
58651 NY10, NY10-260E 3082 B B B Gag 253 262 p24(121-130) 1546..1575 B*3501 NPPIPVGEIY NPPIPVGdIY E8D E260D SF, SSF susceptible form, subtype-specific susceptible form CD8 T-cell Elispot - IFNy, HLA binding, Intracellular cytokine staining, Tetramer binding The B clade variant, NPPIPVGdIY, is also the major C clade form of epitope NY10. This NY10-260D variant binds to HLA-B*3105 10x better than the Clade B wt and is 3x more stable. Matthews2012
230   380       Gag 253 267 p24(121-135) 1546..1590 B8 NPPIPVGEIYKRWII NPPIPVGdIYKRWII E8D E260D SF susceptible form   This variant was recognized by patient CTLs, but the wt epitope was not recognized, indicating that the CTLs tested were of different population than those raised against the wt epitope. Goulder1997ePhillips1991
57725   2626       Gag 253 272 p24(121-140) 1546..1605   NPPIPVGEIYKRWIILGLNK NPPIPVGEIYKRWIImGLNK L16M L268M SF susceptible form CD8 T-cell Elispot - IFNy, Sequence Variant NPPIPVGEIYKRWIImGLNK was seen in patient C07. Vollbrecht2010
242   1544 B B A Gag 254 262 p24(122-130) 1549..1575 B35 PPIPVGEIY PPIPVGdIY E7D E260D SF susceptible form Chromium-release assay One HEPS Kenyan subject cross-reacted to this B clade epitope but elicited a stronger reaction to the A clade form, PPIPVGdIY. Rowland-Jones1998
56011 PY9(p24) 1909 B B B Gag 254 262 p24(122-130) 1549..1575   PPIPVGEIY PPIPVGdIY E7D E260D OV observed variant CD8 T-cell Elispot - IFNy, Sequence This Asian B Clade optimal epitope differs from the consensus B at one position. It is predicted to be HLA-B35 restricted. Experimentally, B clade consensus peptide was used to challenge CTL response in subjects commonly carrying the Asian B-type epitope. Zhai2008
56011 PY9(p24) 1910 B B B Gag 254 262 p24(122-130) 1549..1575   PPIPVGEIY NPVPVGNIY P1N, I3V, E7N P254N, I256V, E260N OV observed variant CD8 T-cell Elispot - IFNy, Sequence This Asian B Clade optimal epitope differs from the consensus B at 3 residues. Experimentally, B clade consensus peptide was used to challenge CTL response in subjects commonly carrying the Asian B-type epitope. Zhai2008
58389 Peptide 63 2922 C C C Gag 254 268 p24(122-136) 1549..1593   PPIPVGDIYKRWIIL PPvPVGeIYKRWIIL I3V, D7E I256V, D260E SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Chinese Clade-C peptide 63, PPvPVGeIYKRWIIL, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58389 Peptide 63 2923 C C C Gag 254 268 p24(122-136) 1549..1593   xPPIPVGDIYKRWII nPPIPVGeIYKRWII x1N, D8E x254N, D261E SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Consensus Clade-B peptide 63, nPPIPVGeIYKRWII, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
58389 Peptide 63 2924 C C D Gag 254 268 p24(122-136) 1549..1593   PPIPVGDIYKRWIIL PPIPVGeIYKRWIIL D7E D260E SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy, Sequence Chinese Clade-D peptide 63, PPIPVGeIYKRWIIL, cross reacted to elicit a response from South African subjects carrying clade-C virus. Zembe2011
254   1110   B   Gag 259 267 p24(127-135) 1564..1590 B*0801 GDIYKRWII GeIYKRWII D2E D260E SSF subtype-specific susceptible form Chromium-release assay A peptide containing this circulating Ugandan variant was recognized as well by a CTL clone from a Clade B-infected patient. McAdam1998
252   1345       Gag 259 267 p24(127-135) 1564..1590 B8 GEIYKRWII GdIYKRWII E2D E260D E escape documented in this paper CD8 T-cell Elispot - IFNy, Chromium-release assay, HLA binding, Longitudinal study Both E index epitope and D variant bind HLA-B8 similarly. The E index loses recognition by CTL coincident with its emergence as the only detectable form, though later it is recognized again. This appears to be an example of escape from CTL response when the circulating CTL clones fail to recognize the form they are specific for. The latter return of recognition of the E form is thought to be a cross-reactive response. Nowak1995
55007 GEI 1805       Gag 259 267 p24(127-135) 1564..1590 B*0801 GEIYKRWII GdIYrRWII E2D, K5R E260D, K263R NSF non-susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding None of the patients tested responded to this variant. Turnbull2006
55007 GEI 1806       Gag 259 267 p24(127-135) 1564..1590 B*0801 GEIYKRWII rkIYKRWII G1R, E2K G259R, E260K NSF non-susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding None of the patients tested responded to this variant. Turnbull2006
55007 GEI 1807       Gag 259 267 p24(127-135) 1564..1590 B*0801 GEIYKRWII GdIYrkWIv E2D, K5R, R6K, I9V E260D, K263R, R264K, I267V NSF non-susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding None of the patients tested responded well to this variant. Turnbull2006
55007 GEI 1808       Gag 259 267 p24(127-135) 1564..1590 B*0801 GEIYKRWII GnIYrRWIq E2N, K5R, I9Q E260N, K263R, I267Q NSF non-susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding None of the patients tested responded to this variant. Turnbull2006
55007 GEI 1809       Gag 259 267 p24(127-135) 1564..1590 B*0801 GEIYKRWII GEIYKRWIv I9V I267V DR, SF diminished response, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding Some patients had response at the level of the response to the index peptide. 2 patients had about 50% of the original response. Turnbull2006
55007 GEI 1810       Gag 259 267 p24(127-135) 1564..1590 B*0801 GEIYKRWII GdIYKRWII E2D E260D DR, SF diminished response, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding Some patients had response at the level of the response to the index peptide. 2 patients had about 50% of the original response. Turnbull2006
55007 GEI 1811       Gag 259 267 p24(127-135) 1564..1590 B*0801 GEIYKRWII GdIYKRWIv E2D, I9V E260D, I267V DR, NSF, SF diminished response, non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy, Tetramer binding One patient responded at 80% of original response, 2 at 60%, 1 at 40% and 1 at 10%. Turnbull2006
57493 GI9 2480 B B B Gag 259 267 p24(127-135) 1564..1590   GEIYKRWII GdIYKRWII E2D E260D SF susceptible form CD8 T-cell Elispot - IFNy Patients 2275 (Latin male, experienced some treatment, autologous virus Clade B); 2792 (Caucasian female, treatment naive, autologous virus Clade B); 2902 (Caucasian male, treated, autologous virus Clade B) all continued to elicit CTL response to variant GdIYKRWII. Hoof2010
57493 GI9 2481 B B B Gag 259 267 p24(127-135) 1564..1590   GEIYKRWII GEIYKRWIv I9V I267V SF susceptible form CD8 T-cell Elispot - IFNy Patients 2275 (Latin male, experienced some treatment, autologous virus Clade B); 2792 (Caucasian female, treatment naive, autologous virus Clade B); 2902 (Caucasian male, treated, autologous virus Clade B) all continued to elicit CTL response to variant GEIYKRWIv. Hoof2010
57493 GI9 2482 B B B Gag 259 267 p24(127-135) 1564..1590   GEIYKRWII GEIYKaWII R6A R264A NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patients 2275 (Latin male, experienced some treatment, autologous virus Clade B); 2792 (Caucasian female, treatment naive, autologous virus Clade B) both continued to elicit CTL response to variant GEIYKaWII, but patient 2902 (Caucasian male, treated, autologous virus Clade B) did not elicit a response upon encountering this variant. Hoof2010
57493 GI9 2483 B B B Gag 259 267 p24(127-135) 1564..1590   GEIYKRWII GEIYaRWII K5A K263A NSF non-susceptible form CD8 T-cell Elispot - IFNy All 3 patients, 2275 (Latin male, experienced some treatment, autologous virus Clade B); 2792 (Caucasian female, treatment naive, autologous virus Clade B); 2902 (Caucasian male, treated, autologous virus Clade B) did not elicit CTL responses to variant GEIYaRWII. Hoof2010
57493 GI9 2484 B B B Gag 259 267 p24(127-135) 1564..1590   GEIYKRWII GEIaKRWII Y4A Y262A NSF, SF non-susceptible form, susceptible form CD8 T-cell Elispot - IFNy Patient 2792 (Caucasian female, treatment naive, autologous virus Clade B) both continued to elicit CTL response to variant GEIaKRWII, but patients 2902 (Caucasian male, treated, autologous virus Clade B) and 2275 (Latin male, experienced some treatment, autologous virus Clade B)did not elicit a response upon encountering this variant. Hoof2010
57493 GI9 2485 B B B Gag 259 267 p24(127-135) 1564..1590   GEIYKRWII GEIYrRWII K5R K263R SF susceptible form CD8 T-cell Elispot - IFNy Patients 2275 (Latin male, experienced some treatment, autologous virus Clade B); 2792 (Caucasian female, treatment naive, autologous virus Clade B); 2902 (Caucasian male, treated, autologous virus Clade B) all continued to elicit CTL response to variant GEIYrRWII. Hoof2010
53630   116 B     Gag 260 267 p24(128-135) 1567..1590 B8 EIYKRWII dIYKRWII E1D E260D NSF non-susceptible form Flow cytometric T-cell cytokine assay, Intracellular cytokine staining Diykrwii sequence was found in 12/17 clones after the initiation of therapy, while eVykrwii sequence was found in 5/17, and the peptide used to initially detect the response was not found, EIYKRWII. The less frequent clone was most often recognized. No dramatic shift towards escape was observed after the initiation of therapy. Casazza2005a
53630   117 B     Gag 260 267 p24(128-135) 1567..1590 B8 EIYKRWII EvYKRWII I2V I261V SF susceptible form Flow cytometric T-cell cytokine assay, Intracellular cytokine staining Diykrwii sequence was found in 12/17 clones after the initiation of therapy, while eVykrwii sequence was found in 5/17, and the peptide used to initially detect the response was not found, EIYKRWII. The less frequent clone was most often recognized. No dramatic shift towards escape was observed after the initiation of therapy. Casazza2005a
52925 E18 182 B     Gag 260 267 p24(128-135) 1567..1590 B8 EIYKRWII dIYKRWII E1D E260D SF susceptible form   3 subjects recognized this epitope with intermediate functional avidity. Autologous sequence revealed one substitution, Diyrkwil, in 1 of the 3; this version of the epitope also had intermediate functional avidity with the donor's cells. Draenert2004b
53743   505       Gag 260 267 p24(128-135) 1567..1590 B8 EIYRKWII EfYRKWII I2F I261F OV observed variant   Variant was found in 1/5 B57+ individuals, but was always in a minor form. The frequency of the epitope mutation did not correlate with the percentage of IFN-gamma producing CTLs. Jansen2005a
53743   506       Gag 260 267 p24(128-135) 1567..1590 B8 EIYRKWII rIYRKWII E1R E260R OV observed variant   Variant was found in 1/5 B57+ individuals, but was always in a minor form. The frequency of the epitope mutation did not correlate with the percentage of IFN-gamma producing CTLs. Jansen2005a
53749 EI8 759 B     Gag 260 267 p24(128-135) 1567..1590 B8 EIYKRWII dIYKRWII E1D E260D SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay This variant was the only form of the epitope detected over a 5 year time period in a patient. The variant was equally well recognized by patient CTLs as the wt consensus B epitope. Koibuchi2005a
54536 EI8 1024 B B A, C Gag 260 267 p24(128-135) 1567..1590 B8 EIYKRWII dIYKRWII E1D E260D SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy Cross-recognition is seen to both A- and C-clade variants. Both variants contain a change at position 1 to dIYKRWII. Malhotra2007
58193 EI8 2857   B B Gag 260 267 p24(128-135) 1567..1590 B*08 EIYKRWII dIYKRWII E1D E260D LE literature escape Intracellular cytokine staining dIYKRWII was one of 2 EI8 sequence variants cross-recognized by subdominant clonotypes. Conrad2011
58193 EI8 2858   B B Gag 260 267 p24(128-135) 1567..1590 B*08 EIYKRWII EIYKRWIv I8V I267V LE literature escape Intracellular cytokine staining EIYKRWIv was one of 2 EI8 sequence variants cross-recognized by subdominant clonotypes. Conrad2011
53925   57       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KkWIImGLNK R2K, L6M R264K, L268M DHB, E diminished HLA binding or increased off-rate, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Previously reported escape (R2K) variant, confirmed here by lack of EliSpot response in 4 individuals and 348-fold decrease in binding to HLA B27. Ammaranond2005
53925   58       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KqWIImGLNK R2Q, L6M R264Q, L268M DHB, E diminished HLA binding or increased off-rate, escape documented in this paper CD8 T-cell Elispot - IFNy, HLA binding Novel escape variant (R2Q), confirmed by lack of EliSpot response in 4 individuals and 30-fold decrease in binding to HLA B27. The escape mutation is R2Q, since HLA binding to KRWIImGLNK is comparable to KRWIILGLNK binding. Ammaranond2005
53619 KK10 75 B     Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KgWIILGLNK R2G R264G E escape documented in this paper Chromium-release assay The infecting virus escaped the vaccine-induced T-cell response with an R264G substitution, KgWIILGLNK, which diminishes binding to B27, between the second and third year of infection. Betts2005
52329   133 CRF01_AE B, C, D, F, G A Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KRWmILGLNK I4M I266M SSF subtype-specific susceptible form CD8 T-cell Elispot - IFNy Subject AIHP-6 (Thai, CDF01-AE infected) recognized this epitope. This subject showed cross-subtype CTL responses to gag constructs derived from subtypes A, B, C, D, F, G, and H, and this epitope was perfectly preserved in all of these but subtype A which had the sequence KRWMILGLNK. This subject didn't respond to a Gag CRF01 sequence which had a R->K mutation in position 2. Currier2002b
52329   134 CRF01_AE B, C, D, F, G CRF01_AE Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KkWIILGLNK R2K R264K SNSF subtype-specific non-susceptible form CD8 T-cell Elispot - IFNy Subject AIHP-6 (Thai, CDF01-AE infected) recognized this epitope. This subject showed cross-subtype CTL responses to gag constructs derived from subtypes A, B, C, D, F, G, and H, and this epitope was perfectly preserved in all of these but subtype A which had the sequence KRWMILGLNK. This subject didn't respond to a Gag CRF01 sequence which had a R->K mutation in position 2. Currier2002b
56266   194 B     Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KgWIILGLNK R2G R264G LE literature escape   Mutation of the peptide sequence EIYKRWIILGLNK to dIYKgWIILGLNK was seen only in 1 subject who exhibited delayed progression to viremia and who initiated ART, but succumbed to non-AIDS death at age 83. This is escape mutant was characterized previously. Dyer2008
52932 KK10 195       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KtWIILGLNK R2T R264T E escape documented in this paper CD8 T-cell Elispot - IFNy Viral load in a perinatally infected child remained low until emergence of an escape variant (kTwiilglnk) in the immunodominant CTL epitope KRWIILGLNK when the child was 7.4 years old. The emergence of this escape mutation was followed by an increase in viremia and an increase in the number of targeted CTL epitopes, measured again when the child was 9.2 years old. The timing suggests that the loss of recognition of this epitope may have resulted in the subsequent loss of immune control. Feeney2004
54618 KK10 254 B     Gag 263 272 p24(131-140) 1576..1605 B*27 KRWIILGLNK KkWIILGLNK R2K R264K CE calculated escape   The variant was more often found in HLA-matched than in HLA-unmatched patients, indicating that some favourable HLA alleles induce strong pressure, resulting in escape variants with high fitness cost and low viral loads. Frater2007
54618 KK10 255 B     Gag 263 272 p24(131-140) 1576..1605 B*27 KRWIILGLNK KRWIImGLNK L6M L268M CE calculated escape   The variant was more often found in HLA-matched than in HLA-unmatched patients, indicating that some favourable HLA alleles induce strong pressure, resulting in escape variants with high fitness cost and low viral loads. Leucine at position 6 was under strong positive selection pressure. Frater2007
54618 KK10 256 B     Gag 263 272 p24(131-140) 1576..1605 B*27 KRWIILGLNK KRWvImGLNK I4V, L6M I266V, L268M OV observed variant   Found in European cohort Frater2007
54618 KK10 257 B     Gag 263 272 p24(131-140) 1576..1605 B*27 KRWIILGLNK KkWIImGLNK R2K, L6M R264K, L268M OV observed variant   Found in European cohort Frater2007
54618 KK10 258 B     Gag 263 272 p24(131-140) 1576..1605 B*27 KRWIILGLNK KRWIIiGLNK L6I L268I CE calculated escape   The variant was more often found in HLA-matched than in HLA-unmatched patients, indicating that some favourable HLA alleles induce strong pressure, resulting in escape variants with high fitness cost and low viral loads. Leucine at position 6 was under strong positive selection pressure. Frater2007
283   367       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIIMGLNK KkWIIMGLNK R2K R264K DHB, E diminished HLA binding or increased off-rate, escape documented in this paper Chromium-release assay, HLA binding Two patients switched to this epitope form during a rapid decline to AIDS. The switch results in severely diminished binding to the B27 and abrogated recognition by CTLs. The switch coincided with rapid CD4 count decline and a rapid rise in viral load. This escape variant is not found in B*2705 negative patients. Goulder1997bGoulder1997e
283   368       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIIMGLNK KRWIIiGLNK M6I M268I E escape documented in this paper Chromium-release assay Variant found in one patient. It was not recognized by CTLs. The escape variant disappeared after initiation of ART. Goulder1997bGoulder1997e
283   369       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIIMGLNK KRWIIlGLNK M6L M268L SF susceptible form Chromium-release assay, HLA binding Variant bound to B*2705 with similar efficiency as the wt epitope. Goulder1997bGoulder1997e
283   370       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIIMGLNK KkWIIlGLNK R2K, M6L R264K, M268L E escape documented in this paper Chromium-release assay, HLA binding Variant had severely diminished binding to B*2705 comparable to the R/K escape variant. Goulder1997bGoulder1997e
271   371 B     Gag 263 272 p24(131-140) 1576..1605 B27, B*2705 KRWIILGLNK KkWIILGLNK R2K R264K E escape documented in this paper   Variant is not recognized by CTLs. Goulder1997dGoulder1997e
271   372 B     Gag 263 272 p24(131-140) 1576..1605 B27, B*2705 KRWIILGLNK KRWIImGLNK L6M L268M OV observed variant   Variant observed in 2/32 clade B sequences in the HIV database. Goulder1997dGoulder1997e
279   381       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KRWIImGLNK L6M L268M SF susceptible form   This variant was recognized more efficiently than the wt epitope by patient CTLs. Goulder1997ePhillips1991
1818 KK10 390       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KRWIImGLNK L6M L268M CM compensatory mutation HLA binding Assumed compensatory mutation. Variant found in one B27 positive child but not in its B27 negative mother. Variant bound to B27 as well as the wt. Goulder2001c
1818 KK10 391       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KkWIILGLNK R2K R264K DHB diminished HLA binding or increased off-rate HLA binding Variant bound to B27 poorly compared to the wt. Goulder2001c
1818 KK10 392       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KkWIImGLNK R2K, L6M R264K, L268M DHB diminished HLA binding or increased off-rate HLA binding Variant bound to B27 poorly compared to the wt. Goulder2001c
1818 KK10 393       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KtWIILGLNK R2T R264T DHB diminished HLA binding or increased off-rate CD8 T-cell Elispot - IFNy The variant was found in mothers and their infected children. There was no CTL response to the wt or the variant in mothers or in children. The variant failed to bind B27. Variant was replication competent. Goulder2001c
1818 KK10 394       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KtWIImGLNK R2T, L6M R264T, L268M CM, DHB compensatory mutation, diminished HLA binding or increased off-rate CD8 T-cell Elispot - IFNy The variant was found in mothers and their infected children. There was no CTL response to the wt or the variant in mothers or in children. The variant failed to bind B27. The variant had presumed compensatory L/M mutation Goulder2001c
1681   675       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KRWIImGLNK L6M L268M SF susceptible form CD8 T-cell Elispot - IFNy Responses to the epitope and the variant were much higher after HIV-1 seroconversion of previous HEPS. Kaul2001a
1352   729       Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KkWIILGLNK R2K R264K OV observed variant Tetramer binding This variant was found in only 2/329 sequences, as R/K mutation was strongly associated with L/M mutation. This mutation occurs rarely in clade B viruses. Position under positive selection pressure. Kelleher2001
1352   730       Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KRWIImGLNK L6M L268M CM compensatory mutation Tetramer binding Variant was present in 1/25 of the viral sequences 52 weeks after infection in one of the patients. Mutation occurs relatively early in the infection. L/M may be a compensatory mutation. Kelleher2001
1352   731       Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KiWIImGLNK R2I, L6M R264I, L268M OV observed variant   This variant was found in one of the patients in 4% of the sequences 1 year after initial infection. Kelleher2001
1352   732       Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KkWIImGLNK R2K, L6M R264K, L268M DHB, IE diminished HLA binding or increased off-rate, inferred escape Tetramer binding Variant was present in 96% of the viral sequences 52 weeks after infection in one of the patients, and after 12 weeks in another, following L/M variant. The two mutations are strongly linked. Substitution reduced binding to B27 and occurred in conjunction with high viral loads. Kelleher2001
55103 KK10 949 B     Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KRWIImGLNK L6M L268M DR, E, TCR diminished response, escape documented in this paper, TCR related mutation CD8 T-cell Elispot - IFNy Mutation does not affect binding to HLA, peptide processing, or viral fitness. Variant was very poorly recognized by KK10-specific CTLs, but it recruited an alternative TCRalpha and beta during chronic infection, being immunogenic enough to elicit a de novo CTL response. Also, enhanced binding of HLA-B*2705-KK10-L6M complex to Immunoglobulin-like transcript-4 (ILT4) occurred, resulting in an impairment of DC maturation and function as measured by the markers HLA-DR, CD83, CD40, CD180 and CD86. Lichterfeld2007a
55103 KK10 950 B     Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KkWIILGLNK R2K R264K DR diminished response CD8 T-cell Elispot - IFNy Variant was recognized by CTLs, but the avidity of recognition decreased by ˜10-fold. Lichterfeld2007a
55103 KK10 951 B     Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KtWIILGLNK R2T R264T DR diminished response CD8 T-cell Elispot - IFNy Variant was recognized by CTLs, but the avidity of recognition decreased by ˜10-fold. Lichterfeld2007a
55103 KK10 952 B     Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KkWIImGLNK R2K, L6M R264K, L268M DR, E diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy Variant was very poorly recognized by CTLs. Lichterfeld2007a
55103 KK10 953 B     Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KtWIImGLNK R2T, L6M R264T, L268M DR, E diminished response, escape documented in this paper CD8 T-cell Elispot - IFNy Variant was very poorly recognized by CTLs. Lichterfeld2007a
281   1346       Gag 263 272 p24(131-140) 1576..1605 B27 KRWIIMGNK KRWIIlGNK M6L M268L SF susceptible form CD8 T-cell Elispot - IFNy, Chromium-release assay, HLA binding, Longitudinal study The M variant is the predominant form, but both M and L forms are recognized by patient CTL. Nowak1995
53834   1417 B     Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KqWIIiGLNK R2Q, L6I R264Q, L268I LE literature escape Sequence This variant was seen in an HLA-B27 carrying father, and it was passed on to the non-B27-mother. Pillay2005
53834   1418 B     Gag 263 272 p24(131-140) 1576..1605 B27 KRWIILGLNK KqWvImGLNK R2Q, I4V, L6M R264Q, I266V, L268M OV observed variant Sequence This variant arose in a non-B27 mother and it was transmitted to the infant who did carry the restricting HLA allele, B27. Pillay2005
55101 KK10 1593 B     Gag 263 272 p24(131-140) 1576..1605   KRWIILGLNK KkWIILGLNK R2K R264K RCR replicative capacity reduced Relative replication capacity assay This R264K mutation abrogates replicative capacity of the virus. Decreased replication is seen under the influence of Cyclophilin A, while increased replication is seen when treated with Cyclosporin A. Schneidewind2007
55101 KK10 1594 B     Gag 263 272 p24(131-140) 1576..1605   KRWIILGLNK KRWIImGLNK L6M L268M RCOK replicative capacity is not abrogated Relative replication capacity assay This L268M mutation does not affect replicative capacity of the virus. Schneidewind2007
55101 KK10 1595 B     Gag 263 272 p24(131-140) 1576..1605   KRWIILGLNK KkWIImGLNK R2K, L6M R264K, L268M RCR replicative capacity reduced Relative replication capacity assay This R264K, L268M mutation abrogates replicative capacity of the virus. Increased replication is seen when treated with Cyclosporin A. Schneidewind2007
55745 KK10 1596 B     Gag 263 272 p24(131-140) 1576..1605 B*2705 KRWIILGLNK KkWIILGLNK R2K R264K DHB, RCR diminished HLA binding or increased off-rate, replicative capacity reduced HLA binding, Relative replication capacity assay