ArticleAIDS (London, England)2013
HLA-A*68:02-restricted Gag-specific cytotoxic T lymphocyte responses can drive selection pressure on HIV but are subdominant and ineffective.
Article in AIDS (London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Characterization of GH18 chitinase in Leishmania braziliensis: expression, structural insights, and implications for vaccine and therapeutic development.Biological research · 2026Article
- HIV infection and ART exposure affect tumor TCR repertoire of diffuse large B cell lymphoma.JCI insight · 2024Article
- No Difference in the Prevalence of HIV-1Vaccines · 2023Article
- Role of HIV-specific CD8The Journal of experimental medicine · 2017Article
- The HIV-1 antisense protein (ASP) induces CD8 T cell responses during chronic infection.Retrovirology · 2015Article
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12 authors at 5 institutions in 4 countries.
Funding
Abstract
backgroundHuman leukocyte allele (HLA) class I polymorphism has the greatest impact of human genetic variation on viral load set point. A substantial part of this effect is due to the action of HLA-B and HLA-C alleles. With few exceptions the role of HLA-A molecules in immune control of HIV is unclear.
methodsWe here study HLA-A*68:02, one of the most highly prevalent HLA-A alleles in C-clade infected sub-Saharan African populations, and one that plays a prominent role in the HIV-specific CD8 T-cell responses made against the virus.
resultsWe define eight epitopes restricted by this allele and propose the peptide binding motif for HLA-A*68:02. Although one of these epitopes almost exactly overlaps an HLA-B*57-restricted epitope in Gag linked with immune control of HIV, this HLA-A*68:02-restricted Gag-TA10 response imposed only weak selection pressure on the virus and was not associated with significantly lower viral setpoint. The only HLA-A*68:02-restricted responses imposing strong selection pressure on HIV were in the flanking regions of Pol-EA8 and Pol-EA11 and within the Vpr-EV10 epitope (P = 8 × 10). However, targeting of this latter epitope was associated with significantly higher viral loads (P = 0.003), suggesting lack of efficacy.
conclusionThis study is consistent with previous data showing that HLA-A-restricted Gag-specific responses can impose selection pressure on HIV. In the case of HLA-A*68:02 the Gag response is subdominant, and apparently has little impact in natural infection. However, these data suggest the potential for high frequency vaccine-induced Gag responses restricted by this allele to have significant antiviral efficacy in vaccine recipients.
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