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HIV Molecular Immunology Database

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Displaying record number 57182

HXB2 Location  Gag(77-85)   Gag Epitope Map
View variants at this location
Epitope SLYNTVATL   Epitope Alignment
Variants
SLYNTVAvL   diminished HLA binding or increased off-rate; escape documented in this paper; literature escape; susceptible form
{k}SLfNTVAvL   literature escape
{k}SLfNTiAvL   literature escape
{k}SLYNTVATL   literature escape
SLfNTVATL   escape documented in this paper; literature escape; susceptible form
{k}SLfNTiATL   literature escape
{k}SLfNTVATL   literature escape
SLYNTiATL   diminished HLA binding or increased off-rate; diminished response; escape documented in this paper; literature escape; susceptible form
SLYNTiAvL   diminished HLA binding or increased off-rate; escape documented in this paper; literature escape; susceptible form
Epitope Name SL9
Species (MHC/HLA human(A*02:01)

Variant Details

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
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.

References

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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