ArticleJournal of virology2007
Escape from the dominant HLA-B27-restricted cytotoxic T-lymphocyte response in Gag is associated with a dramatic reduction in human immunodeficiency virus type 1 replication.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 223 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
223 citing papers in PubMed, 313 citations in OpenAlex.
- Focusing HIV-1 Gag T cell responses to highly conserved regions by DNA vaccination in HVTN 119.JCI insight · 2024Trial
- HLA-B*14:02-Restricted Env-Specific CD8Journal of virology · 2017Trial
- Vaccine-induced gag-specific T cells are associated with reduced viremia after HIV-1 infection.The Journal of infectious diseases · 2013Trial
- Trial
- Rapid antigen processing and presentation of a protective and immunodominant HLA-B*27-restricted hepatitis C virus-specific CD8+ T-cell epitope.PLoS pathogens · 2012Trial
- Role of transmitted Gag CTL polymorphisms in defining replicative capacity and early HIV-1 pathogenesis.PLoS pathogens · 2012Trial
- Trial
- An Ad5-vectored HIV-1 vaccine elicits cell-mediated immunity but does not affect disease progression in HIV-1-infected male subjects: results from a randomized placebo-controlled trial (the Step study).The Journal of infectious diseases · 2011Trial
- Host genetic determinants of T cell responses to the MRKAd5 HIV-1 gag/pol/nef vaccine in the step trial.The Journal of infectious diseases · 2011Trial
- Antiretroviral therapy blocks natural selection on protective and disease-susceptible HLA-B alleles in HIV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- BeyondFrontiers in genetics · 2026Review
- Full-length next-generation sequencing of 11 HLA loci of more than 1000 individuals from clinical cohorts in East and West Africa.bioRxiv : the preprint server for biology · 2025Article
- Consensus Sequences forViruses · 2025Article
- Review
- On the Evolutionary Trajectory of SARS-CoV-2: Host Immunity as a Driver of Adaptation in RNA Viruses.Viruses · 2022Review
- HIV-1 mutants that escape the cytotoxic T-lymphocytes are defective in viral DNA integration.PNAS nexus · 2022Article
- Epitope length variants balance protective immune responses and viral escape in HIV-1 infection.Cell reports · 2022Article
- Article
- HIV-1 capsid variability: viral exploitation and evasion of capsid-binding molecules.Retrovirology · 2021Review
- HIV-1 and human genetic variation.Nature reviews. Genetics · 2021Review
163 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 10 institutions in 4 countries.
Funding
Abstract
Human leukocyte antigen (HLA)-B27-positive subjects are uncommon in their ability to control infection with human immunodeficiency virus type 1 (HIV-1). However, late viral escape from a narrowly directed immunodominant Gag-specific CD8(+) T-lymphocyte (CTL) response has been linked to AIDS progression in these individuals. Identifying the mechanism of the immune-mediated control may provide critical insights into HIV-1 vaccine development. Here, we illustrate that the CTL escape mutation R(264)K in the HLA-B27-restricted KK10 epitope in the capsid resulted in a significant defect in viral replication in vitro. The R(264)K variant was impaired in generating late reverse transcription products, indicating that replication was blocked at a postentry step. Notably, the R(264)K mutation was associated in vivo with the development of a rare secondary mutation, S(173)A, which restored viral replication in vitro. Furthermore, infectivity of the R(264)K variant was rescued by the addition of cyclosporine A or infection of a cyclophilin A-deficient cell line. These data demonstrate a severe functional defect imposed by the R(264)K mutation during an early step in viral replication that is likely due to the inability of this variant to replicate efficiently in the presence of normal levels of cyclophilin A. We conclude that the impact of the R(264)K substitution on capsid structure constrains viral escape and enables long-term maintenance of the dominant CTL response against B27-KK10, providing an explanation for the protective effect of HLA-B27 during HIV infection.
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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.