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Found 13 matching records:

Displaying record number 18

HXB2 Location Gag(20-28) Gag Epitope Map
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Epitope

RLRPGGKKK

Epitope Alignment

Variants

RLRPGGKKc escape documented in this paper

Species (MHC/HLA) human(A*03)

Variant Details

Showing all: 1 variant(s).

Variant ID.	`357`
Epitope Seq.	`RLRPGGKKK`
Variant Seq.	`RLRPGGKKc`
Mutations	K/C
Epitope Location	K9C
HXB2 Location	K28C
Mutation Type	E: escape documented in this paper
Method	Chromium-release assay
Note	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.

References

Goulder1997 P. J. Goulder, A. K. Sewell, D. G. Lalloo, D. A. Price, J. A. Whelan, J. Evans, G. P. Taylor, G. Luzzi, P. Giangrande, R. E. Phillips, and A. J. McMichael. Patterns of Immunodominance in HIV-1-Specific Cytotoxic T Lymphocyte Responses in Two Human Histocompatibility Leukocyte Antigens (HLA)-Identical Siblings with HLA-A*0201 Are Influenced by Epitope Mutation. J. Exp. Med., 8:1423-1433, 1997. Primary human immunodeficiency virus (HIV) infection is controlled principally by HIV-specific cytotoxic T lymphocytes (CTL) to a steady- state level of virus load, which strongly influences the ultimate rate of progression to disease. Epitope selection by CTL may be an important determinant of the degree of immune control over the virus. This report describes the CTL responses of two HLA-identical hemophiliac brothers who were exposed to identical batches of Factor VIII and became seropositive within 10 wk of one another. Both have HLA-A*0201. The CTL responses of the two siblings were very dissimilar, one donor making strong responses to two epitopes within p17 Gag (HLA-A*0201-restricted SLYNTVATL and HLA-A3-restricted RLRPGGKKK). The sibling responded to neither epitope, but made strong responses to two epitopes presented by HLA-B7. This was not the result of differences in presentation of the epitopes. However, mutations in both immunodominant epitopes of the p17 Gag responder were seen in proviral sequences of the nonresponder. We then documented the CTL responses to two HLA-A*0201-restricted epitopes, in Gag (SLYNTVATL) and Pol (ILKEPVHGV) in 22 other HIV-infected donors with HLA-A*0201. The majority (71\%) generated responses to the Gag epitope. In the 29\% of donors failing to respond to the Gag epitope in standard assays, there was evidence of low frequency memory CTL responses using peptide stimulation of PBMC, and most of these donors also showed mutations in or around the Gag epitope. PubMed ID: 9126923. Show all entries for this paper.

Goulder1997e P. Goulder, D. Price, M. Nowak, S. Rowland-Jones, R. Phillips, and A. McMichael. Co-Evolution of Human Immunodeficiency Virus and Cytotoxic T-Lymphocyte Responses. Immunol. Rev., 159:17-29, 1997. PubMed ID: 9416500. Show all entries for this paper.

Displaying record number 49

HXB2 Location Gag(24-35) Gag Epitope Map
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Epitope

GGKKKYKLKHIV

Epitope Alignment

Variants

`GGKKKYKLKHIi`		susceptible form
`GrKKKYKLKHIV`		escape documented in this paper
`GrKKKYKfKHIV`		escape documented in this paper
`rGKKrYKLKHIV`		observed variant
`GGKKqYrLKHIV`		observed variant
`GGKKKYqLKHIV`		observed variant
`GGKKKYaLKHli`		observed variant

Species (MHC/HLA) human(B8)

Variant Details

Showing all: 7 variant(s).

Variant ID.	`373`
Epitope Seq.	`GGKKKYKLKHIV`
Variant Seq.	`GGKKKYKLKHIi`
Mutations	V/I
Epitope Location	V12I
HXB2 Location	V35I
Mutation Type	SF: susceptible form
Note	This variant was recognized as efficiently as the wt epitope by patient CTLs.

Variant ID.	`374`
Epitope Seq.	`GGKKKYKLKHIV`
Variant Seq.	`GrKKKYKLKHIV`
Mutations	G/R
Epitope Location	G2R
HXB2 Location	G25R
Mutation Type	E: escape documented in this paper
Note	This variant failed to be recognized by CTLs and failed to induce target specific lysis.

Variant ID.	`375`
Epitope Seq.	`GGKKKYKLKHIV`
Variant Seq.	`GrKKKYKfKHIV`
Mutations	G/R L/F
Epitope Location	G2R L8F
HXB2 Location	G25R L31F
Mutation Type	E: escape documented in this paper
Note	This variant failed to be recognized by CTLs and failed to induce target specific lysis.

Variant ID.	`376`
Epitope Seq.	`GGKKKYKLKHIV`
Variant Seq.	`rGKKrYKLKHIV`
Mutations	G/R K/R
Epitope Location	G1R K5R
HXB2 Location	G24R K28R
Mutation Type	OV: observed variant
Note	Previously published variants of this epitope.

Variant ID.	`377`
Epitope Seq.	`GGKKKYKLKHIV`
Variant Seq.	`GGKKqYrLKHIV`
Mutations	K/Q K/R
Epitope Location	K5Q K7R
HXB2 Location	K28Q K30R
Mutation Type	OV: observed variant
Note	Previously published variants of this epitope.

Variant ID.	`378`
Epitope Seq.	`GGKKKYKLKHIV`
Variant Seq.	`GGKKKYqLKHIV`
Mutations	K/Q
Epitope Location	K7Q
HXB2 Location	K30Q
Mutation Type	OV: observed variant
Note	Previously published variants of this epitope.

Variant ID.	`379`
Epitope Seq.	`GGKKKYKLKHIV`
Variant Seq.	`GGKKKYaLKHli`
Mutations	I/L V/I K/A
Epitope Location	I11L V12I K7A
HXB2 Location	I34L V35I K30A
Mutation Type	OV: observed variant
Note	Previously published variants of this epitope.

References

Phillips1991 R. E. Phillips, S. Rowland-Jones, D. F. Nixon, F. M. Gotch, J. P. Edwards, A. O. Ogunlesi, J. G. Elvin, J. A. Rothbard, C. R. Bangham, C. R. Rizza, and A. J. McMichael. Human Immunodeficiency Virus Genetic Variation That Can Escape Cytotoxic T Cell Recognition. Nature, 354:453-459, 1991. Fluctuations in the specificity of cytotoxic T-cells for HIV were correlated with variability in proviral gag (DNA) epitope sequences. PubMed ID: 1721107. Show all entries for this paper.

Displaying record number 97

HXB2 Location Gag(77-85) Gag Epitope Map
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Epitope

SLYNTVATL

Epitope Alignment

Variants

`SLhNaVAvL`		escape documented in this paper
`SLfNTVATL`		escape documented in this paper
`SLYNTiAvL`		susceptible form
`SLhNTVATL`		escape documented in this paper
`SLlNTVATL`		observed variant
`SLYNTVAvL`		observed variant
`SLYNTiATL`		observed variant
`SLsNTiATL`		observed variant
`SLfNTVAvL`		observed variant

Epitope Name SL9

Species (MHC/HLA) human(A*02:01)

Variant Details

Showing all: 9 variant(s).

Variant ID.	`358`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLhNaVAvL`
Mutations	Y/H T/A T/V
Epitope Location	Y3H T5A T8V
HXB2 Location	Y79H T81A T84V
Mutation Type	E: escape documented in this paper
Method	Chromium-release assay
Note	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.

Variant ID.	`359`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLfNTVATL`
Mutations	Y/F
Epitope Location	Y3F
HXB2 Location	Y79F
Mutation Type	E: escape documented in this paper
Method	Chromium-release assay
Note	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.

Variant ID.	`360`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLYNTiAvL`
Mutations	V/I T/V
Epitope Location	V6I T8V
HXB2 Location	V82I T84V
Mutation Type	SF: susceptible form
Method	Chromium-release assay
Note	Variant was recognized by CTLs to a similar level as the wt.

Variant ID.	`361`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLhNTVATL`
Mutations	Y/H
Epitope Location	Y3H
HXB2 Location	Y79H
Mutation Type	E: escape documented in this paper
Method	Chromium-release assay
Note	Variant was not recognized by CTLs.

Variant ID.	`362`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLlNTVATL`
Mutations	Y/L
Epitope Location	Y3L
HXB2 Location	Y79L
Mutation Type	OV: observed variant
Note	Variant was found in one epitope responder in 6% of the clones.

Variant ID.	`363`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLYNTVAvL`
Mutations	T/V
Epitope Location	T8V
HXB2 Location	T84V
Mutation Type	OV: observed variant
Note	Variant was found in one epitope responder in 10% of the clones.

Variant ID.	`364`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLYNTiATL`
Mutations	V/I
Epitope Location	V6I
HXB2 Location	V82I
Mutation Type	OV: observed variant
Note	Variant was found in one epitope responder in 9% of the clones.

Variant ID.	`365`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLsNTiATL`
Mutations	Y/S V/I
Epitope Location	Y3S V6I
HXB2 Location	Y79S V82I
Mutation Type	OV: observed variant
Note	Variant was found in one epitope non-responder in 10% of the clones.

Variant ID.	`366`
Epitope Seq.	`SLYNTVATL`
Variant Seq.	`SLfNTVAvL`
Mutations	Y/F T/V
Epitope Location	Y3F T8V
HXB2 Location	Y79F T84V
Mutation Type	OV: observed variant
Note	Variant was found in two epitope non-responders in 25% and 38% of the clones, respectively.

References

Displaying record number 230

HXB2 Location Gag(253-267) Gag Epitope Map
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Epitope

NPPIPVGEIYKRWII

Epitope Alignment

Variants

NPPIPVGdIYKRWII susceptible form

Species (MHC/HLA) human(B8)

Variant Details

Showing all: 1 variant(s).

Variant ID.	`380`
Epitope Seq.	`NPPIPVGEIYKRWII`
Variant Seq.	`NPPIPVGdIYKRWII`
Mutations	E/D
Epitope Location	E8D
HXB2 Location	E260D
Mutation Type	SF: susceptible form
Note	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.

References

Displaying record number 283

HXB2 Location Gag(263-272) Gag Epitope Map
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Epitope

KRWIIMGLNK

Epitope Alignment

Variants

`KkWIIMGLNK`		diminished HLA binding or increased off-rate; escape documented in this paper
`KRWIIiGLNK`		escape documented in this paper
`KRWIIlGLNK`		susceptible form
`KkWIIlGLNK`		escape documented in this paper
`KRWIIMGmNK`		observed variant

Species (MHC/HLA) human(B27)

Variant Details

Showing all: 5 variant(s).

Variant ID.	`367`
Epitope Seq.	`KRWIIMGLNK`
Variant Seq.	`KkWIIMGLNK`
Mutations	R/K
Epitope Location	R2K
HXB2 Location	R264K
Mutation Type	DHB: diminished HLA binding or increased off-rate E: escape documented in this paper
Method	Chromium-release assay, HLA binding
Note	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.

Variant ID.	`368`
Epitope Seq.	`KRWIIMGLNK`
Variant Seq.	`KRWIIiGLNK`
Mutations	M/I
Epitope Location	M6I
HXB2 Location	M268I
Mutation Type	E: escape documented in this paper
Method	Chromium-release assay
Note	Variant found in one patient. It was not recognized by CTLs. The escape variant disappeared after initiation of ART.

Variant ID.	`369`
Epitope Seq.	`KRWIIMGLNK`
Variant Seq.	`KRWIIlGLNK`
Mutations	M/L
Epitope Location	M6L
HXB2 Location	M268L
Mutation Type	SF: susceptible form
Method	Chromium-release assay, HLA binding
Note	Variant bound to B*2705 with similar efficiency as the wt epitope.

Variant ID.	`370`
Epitope Seq.	`KRWIIMGLNK`
Variant Seq.	`KkWIIlGLNK`
Mutations	R/K M/L
Epitope Location	R2K M6L
HXB2 Location	R264K M268L
Mutation Type	E: escape documented in this paper
Method	Chromium-release assay, HLA binding
Note	Variant had severely diminished binding to B*2705 comparable to the R/K escape variant.

Variant ID.	`2211`
Epitope Seq.	`KRWIIMGLNK`
Variant Seq.	`KRWIIMGmNK`
Mutations	L/M
Epitope Location	L8M
HXB2 Location	L270M
Mutation Type	OV: observed variant
Note	Variant observed early on, but coincided with relatively stable CD4 count, viral load, and stable CTL response.

References

Goulder1997b P. J. R. Goulder, R. E. Phillips, R. A. Colbert, S. McAdam, G. Ogg, M. A. Nowak, P. Giangrande, G. Luzzi, B. Morgan, A. Edwards, A. McMichael, and S. Rowland-Jones. Late Escape from an Immunodominant Cytotoxic T-Lymphocyte Response Associated with Progression to AIDS. Nat. Med., 3:212-216, 1997. The CTL response was studied in six HIV+ individuals who make a strong immunodominat response to the same B27 epitope. In two donors an escape mutation arose after close to 10 years of epitope stability, around the time of progression to AIDS. PubMed ID: 9018241. Show all entries for this paper.

Displaying record number 279

HXB2 Location Gag(263-272) Gag Epitope Map
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Epitope

KRWIILGLNK

Epitope Alignment

Variants

KRWIImGLNK susceptible form

Species (MHC/HLA) human(B27)

Variant Details

Showing all: 1 variant(s).

Variant ID.	`381`
Epitope Seq.	`KRWIILGLNK`
Variant Seq.	`KRWIImGLNK`
Mutations	L/M
Epitope Location	L6M
HXB2 Location	L268M
Mutation Type	SF: susceptible form
Note	This variant was recognized more efficiently than the wt epitope by patient CTLs.

References

Displaying record number 271

HXB2 Location Gag(263-272) Gag Epitope Map
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Epitope

KRWIILGLNK

Epitope Alignment

Variants

`KkWIILGLNK`		escape documented in this paper
`KRWIImGLNK`		observed variant

Species (MHC/HLA) human(B*27:05, B27)

Variant Details

Showing all: 2 variant(s).

Variant ID.	`371`
Epitope Seq.	`KRWIILGLNK`
Variant Seq.	`KkWIILGLNK`
Mutations	R/K
Epitope Location	R2K
HXB2 Location	R264K
Mutation Type	E: escape documented in this paper
Note	Variant is not recognized by CTLs.

Variant ID.	`372`
Epitope Seq.	`KRWIILGLNK`
Variant Seq.	`KRWIImGLNK`
Mutations	L/M
Epitope Location	L6M
HXB2 Location	L268M
Mutation Type	OV: observed variant
Note	Variant observed in 2/32 clade B sequences in the HIV database.

References

Goulder1997d P. J. Goulder, A. Edwards, R. E. Phillips, and A. J. McMichael. Identification of a Novel HLA-B*2705-Restricted Cytotoxic T Lymphocyte Epitope within a Conserved Region of HIV-1 Nef. AIDS, 11:536-538, 1997. PubMed ID: 9084804. Show all entries for this paper.

Displaying record number 345

HXB2 Location Gag(323-337) Gag Epitope Map
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Epitope

VQNANPDCKTILKAL

Epitope Alignment

Variants

VQNANPDCrTILKAL escape documented in this paper

Species (MHC/HLA) human(B8)

Variant Details

Showing all: 1 variant(s).

Variant ID.	`382`
Epitope Seq.	`VQNANPDCKTILKAL`
Variant Seq.	`VQNANPDCrTILKAL`
Mutations	K/R
Epitope Location	K9R
HXB2 Location	K331R
Mutation Type	E: escape documented in this paper
Note	This variant failed to be recognized by CTLs and failed to induce target specific lysis.

References

Displaying record number 622

HXB2 Location gp160(31-39) gp160 Epitope Map
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Epitope

AENLWVTVY

Epitope Alignment

Variants

`tENLWVTVY`		susceptible form
`AkNLWVTVY`		non-susceptible form
`AgNLWVTVY`		non-susceptible form
`AaNLWVTVY`		non-susceptible form

Species (MHC/HLA) human(B44)

Variant Details

Showing all: 4 variant(s).

Variant ID.	`91`
Epitope Seq.	`AENLWVTVY`
Variant Seq.	`tENLWVTVY`
Mutations	A/T
Epitope Location	A1T
HXB2 Location	A31T
Mutation Type	SF: susceptible form
Epitope Subtype	B
Variant Subtype	B
Note	The naturally occurring forms of the peptide found in WEAU were tested as targets for early WEAU CTLs -- the form TENLWVTVY was as reactive as the wild type AENLWVTVY -- but the forms AKNLWVTVY, AGNLWVTVY, AANLWVTVY did not serve as targets.

Variant ID.	`92`
Epitope Seq.	`AENLWVTVY`
Variant Seq.	`AkNLWVTVY`
Mutations	E/K
Epitope Location	E2K
HXB2 Location	E32K
Mutation Type	NSF: non-susceptible form
Epitope Subtype	B
Variant Subtype	B
Note	The naturally occurring forms of the peptide found in WEAU were tested as targets for early WEAU CTLs -- the form TENLWVTVY was as reactive as the wild type AENLWVTVY -- but the forms AKNLWVTVY, AGNLWVTVY, AANLWVTVY did not serve as targets.

Variant ID.	`93`
Epitope Seq.	`AENLWVTVY`
Variant Seq.	`AgNLWVTVY`
Mutations	E/G
Epitope Location	E2G
HXB2 Location	E32G
Mutation Type	NSF: non-susceptible form
Epitope Subtype	B
Variant Subtype	B
Note	The naturally occurring forms of the peptide found in WEAU were tested as targets for early WEAU CTLs -- the form TENLWVTVY was as reactive as the wild type AENLWVTVY -- but the forms AKNLWVTVY, AGNLWVTVY, AANLWVTVY did not serve as targets.

Variant ID.	`94`
Epitope Seq.	`AENLWVTVY`
Variant Seq.	`AaNLWVTVY`
Mutations	E/A
Epitope Location	E2A
HXB2 Location	E32A
Mutation Type	NSF: non-susceptible form
Epitope Subtype	B
Variant Subtype	B
Note	The naturally occurring forms of the peptide found in WEAU were tested as targets for early WEAU CTLs -- the form TENLWVTVY was as reactive as the wild type AENLWVTVY -- but the forms AKNLWVTVY, AGNLWVTVY, AANLWVTVY did not serve as targets.

References

Borrow1997 P. Borrow, H. Lewicki, X. Wei, M. S. Horwitz, N. Peffer, H. Meyers, J. A. Nelson, J. E. Gairin, B. H. Hahn, M. B. Oldstone, and G. M. Shaw. Anti-Viral Pressure Exerted by HIV-1-Specific Cytotoxic T Lymphocytes (CTLs) During Primary Infection Demonstrated by Rapid Selection of CTL Escape Virus. Nat. Med., 3:205-211, 1997. Genetic pathways of virus escape from CTL pressure resembled virus escape from antiretroviral therapy. PubMed ID: 9018240. Show all entries for this paper.

Borrow1998 P. Borrow and G. M. Shaw. Cytotoxic T-Lymphocyte Escape Viral Variants: How Important Are They in Viral Evasion of Immune Clearance In Vivo? Immunol. Rev., 164:37-51, 1998. PubMed ID: 9795762. Show all entries for this paper.

Displaying record number 981

HXB2 Location Nef(73-82) Nef Epitope Map
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Epitope

QVPLRPMTYK

Epitope Alignment

Variants

`QVPLRPMTsr`		diminished HLA binding or increased off-rate
`{r*}QVPLRPMTYK{g}`		inferred escape; processing

Species (MHC/HLA) human(A11)

Variant Details

Showing all: 2 variant(s).

Variant ID.	`128`
Epitope Seq.	`QVPLRPMTYK`
Variant Seq.	`QVPLRPMTsr`
Mutations	K/R Y/S
Epitope Location	K10R Y9S
HXB2 Location	K82R Y81S
Mutation Type	DHB: diminished HLA binding or increased off-rate
Method	Chromium-release assay, HLA binding
Note	The epitope QVPLRPMTYK was entirely conserved in 9 isolates from the donor who did not recognize this epitope. QVPLRPMTsr substitutions resulted in a very low binding to HLA-A11.

Variant ID.	`2283`
Epitope Seq.	`{T*}QVPLRPMTYK{A}`
Variant Seq.	`{r*}QVPLRPMTYK{g}`
Mutations	A/G T/R
Epitope Location	A+1G T-2R
HXB2 Location	A83G T71R
Mutation Type	IE: inferred escape P: processing
Method	Chromium-release assay, HLA binding
Note	The epitope QVPLRPMTYK was entirely conserved in 9 isolates from the donor who did not recognize this epitope, whereas there were flanking mutations T71R and A83G, suggesting a processing escape.

References

Couillin1994 I. Couillin, B. Culmann-Penciolelli, E. Gomard, J. Choppin, J. P Levy, J. G. Guillet, and S. Sarasgosti. Impaired Cytotoxic T Lymphocyte Recognition Due to Genetic Variations in the Main Immunogenic Region of the Human Immunodeficiency Virus 1 NEF Protein. J. Exp. Med., 180:1129-11234, 1994. HIV-1 HLA-A11 and -B18 restricted epitopes were sequenced from donors who do and do not express the HLA-A11 and B18 molecule. Selective variations were only detected in virus isolated from individuals expressing the appropriate HLA type. Variant peptides with single substitutions within the minimal epitope did not always completely abrogate HLA binding, suggesting that multiple alterations within a particular epitope may need to accumulate during disease progression to allow viral escape. PubMed ID: 7520468. Show all entries for this paper.

Displaying record number 1007

HXB2 Location Nef(84-92) Nef Epitope Map
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Epitope

AVDLSHFLK

Epitope Alignment

Variants

`AfDLSHFLr`		diminished HLA binding or increased off-rate
`ArDLSHFLK`		diminished HLA binding or increased off-rate
`AlDLSHFLK`		susceptible form

Species (MHC/HLA) human(A11)

Variant Details

Showing all: 3 variant(s).

Variant ID.	`129`
Epitope Seq.	`AVDLSHFLK`
Variant Seq.	`AfDLSHFLr`
Mutations	V/F K/R
Epitope Location	V2F K9R
HXB2 Location	V85F K92R
Mutation Type	DHB: diminished HLA binding or increased off-rate
Method	Chromium-release assay, HLA binding
Note	AfDLSHFLr and ArDLSHFLK mutations abrogated HLA-A11 binding. V to L substitution (AlDLSHFLK) in the second position of the epitope did not influence recognition by HLA-A11 restricted CTL.

Variant ID.	`130`
Epitope Seq.	`AVDLSHFLK`
Variant Seq.	`ArDLSHFLK`
Mutations	V/R
Epitope Location	V2R
HXB2 Location	V85R
Mutation Type	DHB: diminished HLA binding or increased off-rate
Method	Chromium-release assay, HLA binding
Note	AfDLSHFLr and ArDLSHFLK mutations abrogated HLA-A11 binding. V to L substitution (AlDLSHFLK) in the second position of the epitope did not influence recognition by HLA-A11 restricted CTL.

Variant ID.	`131`
Epitope Seq.	`AVDLSHFLK`
Variant Seq.	`AlDLSHFLK`
Mutations	V/L
Epitope Location	V2L
HXB2 Location	V85L
Mutation Type	SF: susceptible form
Method	Chromium-release assay, HLA binding
Note	AfDLSHFLr and ArDLSHFLK mutations abrogated HLA-A11 binding. V to L substitution (AlDLSHFLK) in the second position of the epitope did not influence recognition by HLA-A11 restricted CTL.

References

Displaying record number 1015

HXB2 Location Nef(90-97) Nef Epitope Map
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Epitope

FLKEKGGL

Epitope Alignment

Variants

`FLKEqGGL`		diminished HLA binding or increased off-rate; escape documented in this paper
`FLKEeGGL`		diminished HLA binding or increased off-rate; escape documented in this paper
`FLKEnGGL`		diminished HLA binding or increased off-rate; escape documented in this paper
`FLKdKGGL`		diminished HLA binding or increased off-rate; escape documented in this paper
`sLKEKGGL`		susceptible form
`lLKEKGGL`		susceptible form
`FiKEnGGL`		diminished HLA binding or increased off-rate; escape documented in this paper
`FLeEnGGL`		diminished HLA binding or increased off-rate; escape documented in this paper
`FLKgnGGL`		diminished HLA binding or increased off-rate; escape documented in this paper
`--------`		epitope loss

Species (MHC/HLA) human(B*08)

Variant Details

Showing all: 10 variant(s).

Variant ID.	`1431`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`FLKEqGGL`
Mutations	K/Q
Epitope Location	K5Q
HXB2 Location	K94Q
Mutation Type	DHB: diminished HLA binding or increased off-rate E: escape documented in this paper
Method	Chromium-release assay, HLA binding
Note	Reduced binding and recognition

Variant ID.	`1432`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`FLKEeGGL`
Mutations	K/E
Epitope Location	K5E
HXB2 Location	K94E
Mutation Type	DHB: diminished HLA binding or increased off-rate E: escape documented in this paper
Method	Chromium-release assay, HLA binding
Note	Reduced binding, recognition

Variant ID.	`1433`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`FLKEnGGL`
Mutations	K/N
Epitope Location	K5N
HXB2 Location	K94N
Mutation Type	DHB: diminished HLA binding or increased off-rate E: escape documented in this paper
Method	Chromium-release assay, HLA binding
Note	Reduced binding, recognition

Variant ID.	`1434`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`FLKdKGGL`
Mutations	E/D
Epitope Location	E4D
HXB2 Location	E93D
Mutation Type	DHB: diminished HLA binding or increased off-rate E: escape documented in this paper
Method	Chromium-release assay, HLA binding
Note	Reduced binding, recognition

Variant ID.	`1435`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`sLKEKGGL`
Mutations	F/S
Epitope Location	F1S
HXB2 Location	F90S
Mutation Type	SF: susceptible form
Method	HLA binding
Note	Variant recognized robustly

Variant ID.	`1436`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`lLKEKGGL`
Mutations	F/L
Epitope Location	F1L
HXB2 Location	F90L
Mutation Type	SF: susceptible form
Method	HLA binding
Note	Variant recognized robustly

Variant ID.	`1437`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`FiKEnGGL`
Mutations	L/I K/N
Epitope Location	L2I K5N
HXB2 Location	L91I K94N
Mutation Type	DHB: diminished HLA binding or increased off-rate E: escape documented in this paper
Method	HLA binding
Note	Escaped recognition completely

Variant ID.	`1438`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`FLeEnGGL`
Mutations	K/E K/N
Epitope Location	K3E K5N
HXB2 Location	K92E K94N
Mutation Type	DHB: diminished HLA binding or increased off-rate E: escape documented in this paper
Method	HLA binding
Note	Escaped recognition completely

Variant ID.	`1439`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`FLKgnGGL`
Mutations	E/G K/N
Epitope Location	E4G K5N
HXB2 Location	E93G K94N
Mutation Type	DHB: diminished HLA binding or increased off-rate E: escape documented in this paper
Method	HLA binding
Note	Escaped recognition completely

Variant ID.	`2655`
Epitope Seq.	`FLKEKGGL`
Variant Seq.	`--------`
Mutations	F/- L/- K/- E/- K/- G/- G/- L/-
Epitope Location	F1- L2- K3- E4- K5- G6- G7- L8-
HXB2 Location	F90- L91- K92- E93- K94- G95- G96- L97-
Mutation Type	EL: epitope loss
Epitope Subtype	B
Variant Subtype	B
Method	Sequence
Note	A single nucleotide deletion within DNA resulted in a premature termination of Nef protein 6 amino acids before the epitope FL8. 2 clones with this truncation of protein and epitope loss were found at separate time points.

References

Price1997 D. A. Price, P. J. Goulder, P. Klenerman, A. K. Sewell, P. J. Easterbrook, M. Troop, C. R. Bangham, and R. E. Phillips. Positive Selection of HIV-1 Cytotoxic T Lymphocyte Escape Variants during Primary Infection. Proc. Natl. Acad. Sci. U.S.A., 94:1890-1895, 1997. Cytotoxic T lymphocytes (CTLs) are thought to play a crucial role in the termination of the acute primary HIV-1 syndrome, but clear evidence for this presumption has been lacking. Here we demonstrate positive selection of HIV-1 proviral sequences encoding variants within a CTL epitope in Nef, a gene product critical for viral pathogenicity, during and after seroconversion. These positively selected HIV-1 variants carried epitope sequence changes that either diminished or escaped CTL recognition. Other proviruses had mutations that abolished the Nef epitope altogether. These results provide clear evidence that CTLs exert selection pressure on the viral population in acute HIV-1 infection. PubMed ID: 9050875. Show all entries for this paper.

Displaying record number 1066

HXB2 Location Nef(134-144) Nef Epitope Map
View variants at this location

Epitope

RYPLTFGWCYK

Epitope Alignment

Variants

RYPLcFGWCYK escape documented in this paper

Species (MHC/HLA) human(B18)

Variant Details

Showing all: 1 variant(s).

Variant ID.	`132`
Epitope Seq.	`RYPLTFGWCYK`
Variant Seq.	`RYPLcFGWCYK`
Mutations	T/C
Epitope Location	T5C
HXB2 Location	T138C
Mutation Type	E: escape documented in this paper
Method	Chromium-release assay, HLA binding
Note	Mutants with T5C mutation (RYPLcFGWCYK) evade HLA-B18-restricted CTL responses.