Found 19 matching records:
Displaying record number 55565
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HXB2 Location |
Gag(24-31) p17(24-31) DNA(859..882) |
Gag Epitope Map
|
Author Location |
p17(24-31) |
Epitope |
GGKKKYKL
|
Epitope Alignment
|
Epitope Name |
GL8 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B*08) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B*08-restricted autologous epitope GGKKKYKL elicited CTL responses at the earliest time point, with a reduction in response frequency just before disease progression at the second time point. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55564
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HXB2 Location |
Gag(74-82) p17(74-82) DNA(1009..1035) |
Gag Epitope Map
|
Author Location |
p17(74-82) |
Epitope |
ELKSLFNTI
|
Epitope Alignment
|
Epitope Name |
EI9 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B8) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B8-restricted autologous epitope ELKSLFNTI elicited increasing CTL responses at the last 2 time points. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55562
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record as JSON.
HXB2 Location |
Gag(93-101) p17(93-101) DNA(1066..1092) |
Gag Epitope Map
|
Author Location |
p17(93-101) |
Epitope |
EIKDTKEAL
|
Epitope Alignment
|
Epitope Name |
EL9 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B8) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B8-restricted autologous epitope EIKDTKEAL was able to elicit CTL response only by the last time point. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55558
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record as JSON.
HXB2 Location |
Gag(145-152) p24(13-20) DNA(1222..1245) |
Gag Epitope Map
|
Author Location |
p24(13-20) |
Epitope |
QAISPRTL
|
Epitope Alignment
|
Epitope Name |
QL8 |
Subtype |
B |
Species
(MHC/HLA)
|
human(C*07) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-Cw*07-restricted autologous epitope QAISPRTL only elicited a CTL response at the first time point. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55557
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HXB2 Location |
Gag(181-189) p24(49-57) DNA(1330..1356) |
Gag Epitope Map
|
Author Location |
p24(49-57) |
Epitope |
PQDLNTMLN
|
Epitope Alignment
|
Subtype |
B |
Species
(MHC/HLA)
|
human(Cw7) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-Cw7-restricted autologous epitope PQDLNTMLN failed to generate CTL response. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55566
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record as JSON.
HXB2 Location |
Gag(259-267) p24(127-135) DNA(1564..1590) |
Gag Epitope Map
|
Author Location |
p24(127-135) |
Epitope |
GEIYKRWII
|
Epitope Alignment
|
Epitope Name |
GI9 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B*08) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B*08-restricted autologous epitope GEIYKRWII elicited CTL responses at the earliest time point, with a reduction in response frequency just before disease progression at the second time point and an increase at the third sample point. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55568
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HXB2 Location |
Gag(313-322) p24(181-190) DNA(1726..1755) |
Gag Epitope Map
|
Author Location |
p24(181-190) |
Epitope |
VKNWMTETLL
|
Epitope Alignment
|
Epitope Name |
VL10 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B*08) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B*08-restricted autologous epitope VKNWMTETLL only elicited a CTL response at the first time point. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55548
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record as JSON.
HXB2 Location |
Gag(325-334) p24(193-202) DNA(1762..1791) |
Gag Epitope Map
|
Author Location |
p24(193-201) |
Epitope |
NSNPDCKTIL
|
Epitope Alignment
|
Epitope Name |
NL10 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B*51) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A*01, A*68:01, B*08, B*51, C*07, C*15, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B51-restricted autologous epitope NSNPDCKTIL was able to elicit CTL response only by the last time point.
- HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55540
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HXB2 Location |
Pol(313-321) RT(158-166) DNA(3021..3047) |
Pol Epitope Map
|
Author Location |
RT(158-166) |
Epitope |
AIFQSSMTK
|
Epitope Alignment
|
Epitope Name |
AK9 |
Subtype |
B |
Species
(MHC/HLA)
|
human(A*68:01) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-A*6801-restricted autologous epitope AIFQSSMTK was able to elicit CTL response only by the last time point. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55552
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HXB2 Location |
Pol(448-456) RT(293-301) DNA(3426..3452) |
Pol Epitope Map
|
Author Location |
RT(293-301) |
Epitope |
VPLTREAEL
|
Epitope Alignment
|
Epitope Name |
VL9 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B51) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B51-restricted autologous epitope VPLTREAEL elicited increasing CTL responses at the last 2 time points. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55542
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record as JSON.
HXB2 Location |
Env(416-424) gp120(416-424) DNA(7470..7496) |
Env Epitope Map
|
Author Location |
gp160(416-424) |
Epitope |
LPCRIKQII
|
Epitope Alignment
|
Epitope Name |
gp160 LI9 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B51) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B51-restricted autologous epitope LPCRIKQII elicited CTL responses at the limit of detection for ELISpots at the last 2 time points. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55560
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record as JSON.
HXB2 Location |
Env(586-593) gp41(75-82) DNA(7980..8003) |
Env Epitope Map
|
Author Location |
gp160(586-593) |
Epitope |
YLKDQQLL
|
Epitope Alignment
|
|
|
Show epitope variants
|
Epitope Name |
YL8 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B*08) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B*08-restricted autologous epitope YLKDQQLL elicited CTL responses at the earliest time point, with a reduction in response frequency just before disease progression at the second time point. Viral sequencing showed the emergence of an escape variant K3R, YLrDQQLL, between the first 2 ELISpot samplings. By the third time point, neither YL8 sequence was able to elicit an immune response. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55559
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record as JSON.
HXB2 Location |
Env(845-856) gp41(334-345) DNA(8757..8792) |
Env Epitope Map
|
Author Location |
gp160(845-856) |
Epitope |
RRIRQGLERILL
|
Epitope Alignment
|
Epitope Name |
RL12 |
Subtype |
B |
Species
(MHC/HLA)
|
human |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B8-restricted epitope RRIRQGLERILL elicited increasing CTL responses at the last 2 time points. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55563
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HXB2 Location |
Nef(13-20) DNA(8833..8856) |
Nef Epitope Map
|
Author Location |
Nef(13-20) |
Epitope |
WSMVRERM
|
Epitope Alignment
|
Epitope Name |
WM8 |
Subtype |
B |
Species
(MHC/HLA)
|
human |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B8-restricted epitope WSMVRERM was able to elicit CTL response only by the last time point. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55561
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record as JSON.
HXB2 Location |
Nef(90-97) DNA(9064..9087) |
Nef Epitope Map
|
Author Location |
Nef(90-97) |
Epitope |
FLKEMGGL
|
Epitope Alignment
|
Epitope Name |
FL8 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B8) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B8-restricted autologous epitope FLKEMGGL elicited decreasing CTL responses at the last 2 time points. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55556
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record as JSON.
HXB2 Location |
Nef(108-115) DNA(9118..9141) |
Nef Epitope Map
|
Author Location |
Nef(108-115) |
Epitope |
DILDLWVH
|
Epitope Alignment
|
Subtype |
B |
Species
(MHC/HLA)
|
human |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-Cw7-restricted epitope DILDLWVH failed to generate CTL response. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55533
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record as JSON.
HXB2 Location |
Nef(113-128) DNA(9133..9180) |
Nef Epitope Map
|
Author Location |
Nef(113-128) |
Epitope |
WVHHTQGYFPDWQNYT
|
Epitope Alignment
|
Epitope Name |
VT15 |
Subtype |
B |
Species
(MHC/HLA)
|
human |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-A1-restricted epitope WVHHTQGYFPDWQNYT was able to elicit CTL response only by the last time point. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55537
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record as JSON.
HXB2 Location |
Nef(132-147) DNA(9190..9237) |
Nef Epitope Map
|
Author Location |
Nef(132-147) |
Epitope |
GIRYPLTFGWCFKLVP
|
Epitope Alignment
|
Subtype |
B |
Species
(MHC/HLA)
|
human |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ, Other |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-A1 and B8-restricted epitope GIRYPLTFGWCFKLVP failed to generate CTL response. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
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Displaying record number 55570
Download this epitope
record as JSON.
HXB2 Location |
Nef(183-202) DNA(9343..9402) |
Nef Epitope Map
|
Author Location |
Nef |
Epitope |
WKFDSRLAFHHMARELHPEY
|
Epitope Alignment
|
|
|
Show epitope variants
|
Epitope Name |
WY20 |
Subtype |
B |
Species
(MHC/HLA)
|
human(B51) |
Immunogen |
HIV-1 infection |
Patient MHC/HLA |
A1, A*68:01, B51, B8, C*15, Cw7, DQ2, DQ3, DR3, DR4 |
Country |
United States |
Experimental methods |
CD8 T-cell Elispot - IFNγ |
Keywords |
rate of progression, escape, mutation acquisition |
Notes
- An LTNP was followed longitudinally over 6 years and 3 sampling time points, until transition to disease. His HLA were heterozygous and not associated with nonprogressive infection, but 3 alleles were associated with poor clinical prognosis. No attenuating mutations in initial samplings, but an insertion in the V2 loop and continuing CCR5 coreceptor use were found.
- A decrease in IFN-gamma response was seen over time, suggesting CTL dysfunction. An increase in T-cell epitopes targeted (e.g. emergence of YL8, YLKDQQLL and WY20, WKFDSRLAFHHMARELHPEY variants and gain of response to EL9, EIKDTKEAL, NL10, NSNPDCKTIL, AK9, AIFQSSMTK, WM8, WSMVRERM, VT15, WVHHTQGYFPDWQNYT) was seen concomitant with disease progression, reflecting viral replication and/or variants.
- HLA-B51-restricted autolgous peptide epitope WKFDSRLAFHHMARELHPEY (WY20) was tested at the last time point only, eliciting immune responses to both it and an H10R variant, WKFDSRLAFrHMARELHPEY which elicited a decreased CTL response. HLA restriction was predicted in this study based on the patient's HLA alleles and previous publication.
- A Nef AL9 (AFHHMAREL) epitope contained within this peptide did not elicit CTL response even though it is associated with the patient's HLA type.
References
Kemal2008
Kimdar Sherefa Kemal, Tara Beattie, Tao Dong, Barbara Weiser, Rupert Kaul, Carla Kuiken, Julian Sutton, Dorothy Lang, Hongbing Yang, Yan Chun Peng, Ronald Collman, Sean Philpott, Sarah Rowland-Jones, and Harold Burger. Transition from Long-Term Nonprogression to HIV-1 Disease Associated with Escape from Cellular Immune Control. J. Acquir. Immune Defic. Syndr., 48(2):119-126, 1 Jun 2008. PubMed ID: 18520675.
Show all entries for this paper.
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