ArticleThe Journal of experimental medicine2009
Evolution of HLA-B*5703 HIV-1 escape mutations in HLA-B*5703-positive individuals and their transmission recipients.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
133 citing papers in PubMed.
- Killer cell immunoglobulin-like receptor 3DL1 variation modifies HLA-B*57 protection against HIV-1.The Journal of clinical investigation · 2018Trial
- HLA-B*14:02-Restricted Env-Specific CD8Journal of virology · 2017Trial
- Role of transmitted Gag CTL polymorphisms in defining replicative capacity and early HIV-1 pathogenesis.PLoS pathogens · 2012Trial
- Factors associated with viral rebound in HIV-1-infected individuals enrolled in a therapeutic HIV-1 gag vaccine trial.The Journal of infectious diseases · 2011Trial
- Rare variable M. tuberculosis antigens induce predominant Th17 responses in human infection.JCI insight · 2026Article
- No Difference in the Prevalence of HIV-1Vaccines · 2023Article
- Article
- Protective HLA-B57: T cell and natural killer cell recognition in HIV infection.Biochemical Society transactions · 2022Review
- Mechanism of Viral Suppression among HIV Elite Controllers and Long-Term Nonprogressors in Nigeria and South Africa.Viruses · 2022Review
- A longitudinal analysis of immune escapes from HLA-B*13-restricted T-cell responses at early stage of CRF01_AE subtype HIV-1 infection and implications for vaccine design.BMC immunology · 2022Article
- Immunogenetic determinants of heterosexual HIV-1 transmission: key findings and lessons from two distinct African cohorts.Genes and immunity · 2021Review
- Effect of Difference in Consensus Sequence between HIV-1 Subtype A/E and Subtype B Viruses on Elicitation of Gag-Specific CD8Journal of virology · 2021Article
- Article
- Increased Frequency of Inter-Subtype HIV-1 Recombinants Identified by Near Full-Length Virus Sequencing in Rwandan Acute Transmission Cohorts.Frontiers in microbiology · 2021Article
- T-cell responses to sequentially emerging viral escape mutants shape long-term HIV-1 population dynamics.PLoS pathogens · 2020Article
- Specificity of CD8Vaccines · 2020Article
- Accumulated mutations by 6 months of infection collectively render transmitted/founder HIV-1 significantly less fit.The Journal of infection · 2020Article
- Designs of Antigen Structure and Composition for Improved Protein-Based Vaccine Efficacy.Frontiers in immunology · 2020Review
- CD8 T cells targeting adapted epitopes in chronic HIV infection promote dendritic cell maturation and CD4 T cell trans-infection.PLoS pathogens · 2019Article
- Immune Control of HIV.Journal of life sciences (Westlake Village, Calif.) · 2019Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
HLA-B*57 is the class I allele most consistently associated with control of human immunodeficiency virus (HIV) replication, which may be linked to the specific HIV peptides that this allele presents to cytotoxic T lymphocytes (CTLs), and the resulting efficacy of these cellular immune responses. In two HIV C clade-infected populations in South Africa and Zambia, we sought to elucidate the role of HLA-B*5703 in HIV disease outcome. HLA-B*5703-restricted CTL responses select for escape mutations in three Gag p24 epitopes, in a predictable order. We show that the accumulation of these mutations sequentially reduces viral replicative capacity in vitro. Despite this, in vivo data demonstrate that there is ultimately an increase in viral load concomitant with evasion of all three HLA-B*5703-restricted CTL responses. In HLA-B*5703-mismatched recipients, the previously described early benefit of transmitted HLA-B*5703-associated escape mutations is abrogated by the increase in viral load coincident with reversion. Rapid disease progression is observed in HLA-matched recipients to whom mutated virus is transmitted. These data demonstrate that, although costly escape from CTL responses can progressively attenuate the virus, high viral loads develop in the absence of adequate, continued CTL responses. These data underline the need for a CTL vaccine against multiple conserved epitopes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.