ArticleJournal of virology2007
Escape and compensation from early HLA-B57-mediated cytotoxic T-lymphocyte pressure on human immunodeficiency virus type 1 Gag alter capsid interactions with cyclophilin A.
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 197 papers.
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Who cites it
197 citing papers in PubMed, 260 citations in OpenAlex.
- 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
- Short Communication: A Recombinant Variant with Increased Envelope Entry Efficiency Emerged During Early Infection of an HIV-1 Subtype C Dual Infected Rapid Progressor.AIDS research and human retroviruses · 2016Trial
- Vaccine-induced gag-specific T cells are associated with reduced viremia after HIV-1 infection.The Journal of infectious diseases · 2013Trial
- Role of transmitted Gag CTL polymorphisms in defining replicative capacity and early HIV-1 pathogenesis.PLoS pathogens · 2012Trial
- Design of an immunogen containing multidimensionally conserved and immunogenic parts of the HIV proteome.PLoS computational biology · 2026Article
- Predicting the evolutionary and structural compensation in Tat ARM region across HIV-1 groups using machine learning approach.Scientific reports · 2026Article
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- Efficient epistasis inference via higher-order covariance matrix factorization.bioRxiv : the preprint server for biology · 2024Article
- Definition of a New HLA B*52-Restricted Rev CTL Epitope Targeted by an HIV-1-Infected Controller.Viruses · 2023Article
- The apparent interferon resistance of transmitted HIV-1 is possibly a consequence of enhanced replicative fitness.PLoS pathogens · 2022Article
- HIV-1 mutants that escape the cytotoxic T-lymphocytes are defective in viral DNA integration.PNAS nexus · 2022Article
- Next-generation T cell-activating vaccination increases influenza virus mutation prevalence.Science advances · 2022Article
- 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
- HIV-1 capsid variability: viral exploitation and evasion of capsid-binding molecules.Retrovirology · 2021Review
- A participant-derived xenograft model of HIV enables long-term evaluation of autologous immunotherapies.The Journal of experimental medicine · 2021Article
- 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
- Adenovirus-vectored vaccine containing multidimensionally conserved parts of the HIV proteome is immunogenic in rhesus macaques.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- HIV-1Viruses · 2021Article
137 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Certain histocompatibility leukocyte antigen (HLA) alleles are associated with improved clinical outcomes for individuals infected with human immunodeficiency virus type 1 (HIV-1), but the mechanisms for their effects remain undefined. An early CD8(+) T-cell escape mutation in the dominant HLA-B57-restricted Gag epitope TW10 (TSTLQEQIGW) has been shown to impair HIV-1 replication capacity in vitro. We demonstrate here that this T(242)N substitution in the capsid protein is associated with upstream mutations at residues H(219), I(223), and M(228) in the cyclophilin A (CypA)-binding loop in B57(+) individuals with progressive disease. In an independent cohort of epidemiologically linked transmission pairs, the presence of these substitutions in viruses encoding T(242)N was associated with significantly higher plasma viremia in donors, further suggesting that these secondary mutations compensated for the replication defect of T(242)N. Using NL4-3 constructs, we illustrate the ability of these CypA loop changes to partially restore replication of the T(242)N variant in vitro. Notably, these mutations also enhanced viral resistance to the drug cyclosporine A, indicating a reduced dependence of the compensated virus on CypA that is normally essential for optimal infectivity. Therefore, mutations in TW10 allow HIV-1 to evade a dominant early CD8(+) T-cell response, but the benefits of escape are offset by a defect in capsid function. These data suggest that TW10 escape variants undergo a postentry block that is partially overcome by changes in the CypA-binding loop and identify a mechanism for an HIV-1 fitness defect that may contribute to the slower disease progression associated with HLA-B57.
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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.