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Found 2 matching records:

Displaying record number 18

HXB2 Location  Gag(20-28)   Gag Epitope Map
View variants at this location
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 97

HXB2 Location  Gag(77-85)   Gag Epitope Map
View variants at this location
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

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.


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