ArticleJournal of virology2011
Gag cytotoxic T lymphocyte escape mutations can increase sensitivity of HIV-1 to human TRIM5alpha, linking intrinsic and acquired immunity.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- Diverse functions associate with non-coding polymorphisms shared between humans and chimpanzees.BMC ecology and evolution · 2022Article
- HIV-1 capsid variability: viral exploitation and evasion of capsid-binding molecules.Retrovirology · 2021Review
- Differential Inhibition of HIV Replication by the 12 Interferon Alpha Subtypes.Journal of virology · 2021Article
- Editing of the TRIM5 Gene Decreases the Permissiveness of Human T Lymphocytic Cells to HIV-1.Viruses · 2020Article
- Article
- Immune Control of HIV.Journal of life sciences (Westlake Village, Calif.) · 2019Article
- Negative and Positive Selection Pressure During Sexual Transmission of Transmitted Founder HIV-1.Frontiers in immunology · 2019Review
- Defects in assembly explain reduced antiviral activity of the G249D polymorphism in human TRIM5α.PloS one · 2019Article
- A virus-packageable CRISPR screen identifies host factors mediating interferon inhibition of HIV.eLife · 2018Article
- 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
- Restriction Factors: From Intrinsic Viral Restriction to Shaping Cellular Immunity Against HIV-1.Frontiers in immunology · 2018Review
- Targeting TRIM5α in HIV Cure Strategies for the CRISPR-Cas9 Era.Frontiers in immunology · 2017Article
- TRIM5 gene polymorphisms in HIV-1-infected patients and healthy controls from Northeastern Brazil.Immunologic research · 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
- Compensatory substitutions in the HIV-1 capsid reduce the fitness cost associated with resistance to a capsid-targeting small-molecule inhibitor.Journal of virology · 2015Article
- Stabilized human TRIM5α protects human T cells from HIV-1 infection.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- In vivo functions of CPSF6 for HIV-1 as revealed by HIV-1 capsid evolution in HLA-B27-positive subjects.PLoS pathogens · 2014Article
- Pressure from TRIM5α contributes to control of HIV-1 replication by individuals expressing protective HLA-B alleles.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although laboratory-adapted HIV-1 strains are largely resistant to the human restriction factor TRIM5α (hTRIM5α), we have recently shown that some viruses carrying capsid (CA) sequences from clinical isolates can be more sensitive to this restriction factor. In this study we evaluated the contribution to this phenotype of CA mutations known to be associated with escape from cytotoxic T lymphocyte (CTL) responses. Recombinant viruses carrying HIV-1 CA sequences from NL4-3 and three different clinical isolates were prepared, along with variants in which mutations associated with CTL resistance were modified by site-directed mutagenesis, and the infectivities of these viruses in target cells expressing hTRIM5α and cells in which TRIM5α activity had been inhibited by overexpression of TRIM5γ were compared. For both hTRIM5α-sensitive viruses studied, CTL-associated mutations were found to be responsible for this phenotype. Both CTL resistance mutations occurring within HLA-restricted CA epitopes and compensatory mutations occurring outside CTL epitopes influenced hTRIM5α sensitivity, and mutations associated with CTL resistance selected in prior hosts can contribute to this effect. The impact of CTL resistance mutations on hTRIM5α sensitivity was context dependent, because mutations shown to be responsible for the TRIM5α-sensitive phenotype in viruses from one patient could have little or no impact on this parameter when introduced into another virus. No fixed relationship between changes in hTRIM5α sensitivity and infectivity was discernible in our studies. Taken together, these findings suggest that CTL mutations may influence HIV-1 replication by modifying both viral infectivity and sensitivity to TRIM5α.
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