ArticleJournal of virology2013
Pressure from TRIM5α contributes to control of HIV-1 replication by individuals expressing protective HLA-B alleles.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- Computational and Population-Based HLA Permissiveness to HIV Drug Resistance-Associated Mutations.Pathogens (Basel, Switzerland) · 2025Article
- Review
- HIV-1 capsid variability: viral exploitation and evasion of capsid-binding molecules.Retrovirology · 2021Review
- The Landscape of IFN/ISG Signaling in HIV-1-Infected Macrophages and Its Possible Role in the HIV-1 Latency.Cells · 2021Review
- Differential Inhibition of HIV Replication by the 12 Interferon Alpha Subtypes.Journal of virology · 2021Article
- Gut germinal center regeneration and enhanced antiviral immunity by mesenchymal stem/stromal cells in SIV infection.JCI insight · 2021Article
- Editing of the TRIM5 Gene Decreases the Permissiveness of Human T Lymphocytic Cells to HIV-1.Viruses · 2020Article
- Article
- Restriction of HIV-1 and other retroviruses by TRIM5.Nature reviews. Microbiology · 2019Review
- Immune Control of HIV.Journal of life sciences (Westlake Village, Calif.) · 2019Article
- Defects in assembly explain reduced antiviral activity of the G249D polymorphism in human TRIM5α.PloS one · 2019Article
- Genotypic and Mechanistic Characterization of Subtype-Specific HIV Adaptation to Host Cellular Immunity.Journal of virology · 2019Article
- HIV-1 capsids from B27/B57+ elite controllers escape Mx2 but are targeted by TRIM5α, leading to the induction of an antiviral state.PLoS pathogens · 2018Article
- Mechanisms of Virologic Control and Clinical Characteristics of HIV+ Elite/Viremic Controllers.The Yale journal of biology and medicine · 2017Review
- Are Evolution and the Intracellular Innate Immune System Key Determinants in HIV Transmission?Frontiers in immunology · 2017Review
- Targeting TRIM5α in HIV Cure Strategies for the CRISPR-Cas9 Era.Frontiers in immunology · 2017Article
- Nonhuman TRIM5 Variants Enhance Recognition of HIV-1-Infected Cells by CD8+ T Cells.Journal of virology · 2016Article
- CD8+ T Cell Breadth and Ex Vivo Virus Inhibition Capacity Distinguish between Viremic Controllers with and without Protective HLA Class I Alleles.Journal of virology · 2016Article
- Preclinical Assessment of Mutant Human TRIM5α as an Anti-HIV-1 Transgene.Human gene therapy · 2015Article
- Both HLA-B*57 and plasma HIV RNA levels contribute to the HIV-specific CD8+ T cell response in HIV controllers.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of certain HLA class I alleles, including HLA-B*27 and HLA-B*57, is associated with better control of human immunodeficiency virus type 1 (HIV-1) infection, but the mechanisms responsible are not fully understood. We sought evidence that pressure from the human restriction factor TRIM5α (hTRIM5α) could contribute to viral control. The hTRIM5α sensitivity of viruses from both HLA-B*57-positive (HLA-B*57(+)) and HLA-B*27(+) patients who spontaneously controlled viral replication, but not viruses from viremic patients expressing these alleles, was significantly greater than that of viruses from patients not expressing these protective HLA-B alleles. Overall, a significant negative correlation between hTRIM5α sensitivity and viral load was observed. In HLA-B*57(+) patients, the T242N mutation in the HLA-B*57-restricted TW10 CD8(+) T lymphocyte (CTL) epitope was strongly associated with hTRIM5α sensitivity. In HLA-B*27(+) controllers, hTRIM5α sensitivity was associated with a significant reduction in emergence of key CTL mutations. In several patients, viral evolution to avoid hTRIM5α sensitivity was observed but could be associated with reduced viral replicative capacity. Thus, in individuals expressing protective HLA-B alleles, the combined pressures exerted by CTL, hTRIM5α, and capsid structural constraints can prevent viral escape both by impeding the selection of necessary resistance/compensatory mutations and forcing the selection of escape mutations that increase hTRIM5α sensitivity or impair viral replicative capacity.
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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.