Found 1 matching record:
HXB2 Location | Gag(77-85) | Gag Epitope Map
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Epitope |
SLYNTVATL
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Epitope Alignment | ||||||||||||||||||||||||||||
Variants |
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Epitope Name | SL9 | |||||||||||||||||||||||||||||
Species (MHC/HLA) | human(A*02:01) |
Showing all: 9 variant(s).
Variant ID. | 2963 |
---|---|
Epitope Seq. | SLYNTVATL |
Variant Seq. | SLYNTVAvL |
Mutations | T/V |
Epitope Location | T9V |
HXB2 Location | T85V |
Mutation Type | DHB: diminished HLA binding or increased off-rate E: escape documented in this paper LE: literature escape SF: susceptible form |
Epitope Subtype | B |
Variant Subtype | B |
Method | CD8 T-cell Elispot - IFNy, HLA binding, Sequence |
Note | 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. |
Variant ID. | 2965 |
---|---|
Epitope Seq. | {R}SLYNTVATL |
Variant Seq. | {k}SLfNTVAvL |
Mutations | -/K Y/F T/V |
Epitope Location | -1K Y4F T9V |
HXB2 Location | -77K Y80F T85V |
Mutation Type | LE: literature escape |
Epitope Subtype | B |
Variant Subtype | B |
Method | Sequence |
Note | 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. |
Variant ID. | 2966 |
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Epitope Seq. | {R}SLYNTVATL |
Variant Seq. | {k}SLfNTiAvL |
Mutations | -/K Y/F V/I T/V |
Epitope Location | -1K Y4F V7I T9V |
HXB2 Location | -77K Y80F V83I T85V |
Mutation Type | LE: literature escape |
Epitope Subtype | B |
Variant Subtype | B |
Method | Sequence |
Note | 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. |
Variant ID. | 2967 |
---|---|
Epitope Seq. | {R}SLYNTVATL |
Variant Seq. | {k}SLYNTVATL |
Mutations | -/K |
Epitope Location | -1K |
HXB2 Location | -77K |
Mutation Type | LE: literature escape |
Epitope Subtype | B |
Variant Subtype | B |
Method | Sequence |
Note | Epitope {R}SLYNTVATL is seen to vary to {k}SLYNTVATL (SL9-K). |
Variant ID. | 2968 |
---|---|
Epitope Seq. | SLYNTVATL |
Variant Seq. | SLfNTVATL |
Mutations | Y/F |
Epitope Location | Y3F |
HXB2 Location | Y79F |
Mutation Type | E: escape documented in this paper LE: literature escape SF: susceptible form |
Epitope Subtype | B |
Variant Subtype | B |
Method | CD8 T-cell Elispot - IFNy, HLA binding, Longitudinal study |
Note | 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. |
Variant ID. | 2969 |
---|---|
Epitope Seq. | {R}SLYNTVATL |
Variant Seq. | {k}SLfNTiATL |
Mutations | -/K Y/F V/I |
Epitope Location | -1K Y4F V7I |
HXB2 Location | -77K Y80F V83I |
Mutation Type | LE: literature escape |
Epitope Subtype | B |
Variant Subtype | B |
Method | Sequence |
Note | 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. |
Variant ID. | 2970 |
---|---|
Epitope Seq. | {R}SLYNTVATL |
Variant Seq. | {k}SLfNTVATL |
Mutations | -/K Y/F |
Epitope Location | -1K Y4F |
HXB2 Location | -77K Y80F |
Mutation Type | LE: literature escape |
Epitope Subtype | B |
Variant Subtype | B |
Method | Sequence |
Note | CTL selection at TCR contact residues is predicted to drive epitope {k}SLYNTVATL (SL9) to variant, {k}SLfNTVATL (SL9-KF). |
Variant ID. | 2971 |
---|---|
Epitope Seq. | SLYNTVATL |
Variant Seq. | SLYNTiATL |
Mutations | V/I |
Epitope Location | V6I |
HXB2 Location | V82I |
Mutation Type | DHB: diminished HLA binding or increased off-rate DR: diminished response E: escape documented in this paper LE: literature escape SF: susceptible form |
Epitope Subtype | B |
Variant Subtype | B |
Method | CD8 T-cell Elispot - IFNy, HLA binding, Sequence |
Note | 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. |
Variant ID. | 2972 |
---|---|
Epitope Seq. | SLYNTVATL |
Variant Seq. | SLYNTiAvL |
Mutations | V/I T/V |
Epitope Location | V6I T8V |
HXB2 Location | V82I T84V |
Mutation Type | DHB: diminished HLA binding or increased off-rate E: escape documented in this paper LE: literature escape SF: susceptible form |
Epitope Subtype | B |
Variant Subtype | B |
Method | CD8 T-cell Elispot - IFNy, HLA binding, Sequence |
Note | 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 Stefan Tenzer, Edmund Wee, Anne Burgevin, Guillaume Stewart-Jones, Lone Friis, Kasper Lamberth, Chih-hao Chang, Mikkel Harndahl, Mirjana Weimershaus, Jan Gerstoft, Nadja Akkad, Paul Klenerman, Lars Fugger, E. Yvonne Jones, Andrew J. McMichael, Søren Buus, Hansjörg Schild, Peter van Endert, and Astrid K. N. Iversen. Antigen Processing Influences HIV-Specific Cytotoxic T Lymphocyte Immunodominance. Nat. Immunol., 10(6):636-646, Jun 2009. PubMed ID: 19412183. Show all entries for this paper.
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