ArticleMolecular therapy : the journal of the American Society of Gene Therapy2014
Stabilized human TRIM5α protects human T cells from HIV-1 infection.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 35 citations in OpenAlex.
- Updates on the role of TRIM proteins in AIDS: molecular mechanisms and potential for interventions.Frontiers in immunology · 2026Review
- Cyclophilin A Regulates Tripartite Motif 5 Alpha Restriction of HIV-1.International journal of molecular sciences · 2025Review
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- The Humanized Mouse Model: What Added Value Does It Offer for HIV Research?Pathogens (Basel, Switzerland) · 2023Review
- Generation of non-human primate CAR Tregs using artificial antigen-presenting cells, simian tropic lentiviral vectors, and antigen-specific restimulation.STAR protocols · 2022Article
- HIV-1-Infected CD4Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Trafficking and persistence of alloantigen-specific chimeric antigen receptor regulatory T cells in Cynomolgus macaque.Cell reports. Medicine · 2022Article
- Targeting TRIM Proteins: A Quest towards Drugging an Emerging Protein Class.Chembiochem : a European journal of chemical biology · 2021Review
- NPM-ALK-Induced Reprogramming of Mature TCR-Stimulated T Cells Results in Dedifferentiation and Malignant Transformation.Cancer research · 2021Article
- Human TRIM5α: Autophagy Connects Cell-Intrinsic HIV-1 Restriction and Innate Immune Sensor Functioning.Viruses · 2021Review
- HIV-1 Capsid Core: A Bullet to the Heart of the Target Cell.Frontiers in microbiology · 2021Review
- The Interplay of HIV and Autophagy in Early Infection.Frontiers in microbiology · 2021Review
- Mutational resilience of antiviral restriction favors primate TRIM5α in host-virus evolutionary arms races.eLife · 2020Article
- HIV-Resistant and HIV-Specific CAR-Modified CD4Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Ubiquitination and SUMOylation in HIV Infection: Friends and Foes.Current issues in molecular biology · 2020Review
- Restriction of HIV-1 and other retroviruses by TRIM5.Nature reviews. Microbiology · 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
- Improved Expansion andMolecular therapy. Methods & clinical development · 2018Article
- Restriction Factors: From Intrinsic Viral Restriction to Shaping Cellular Immunity Against HIV-1.Frontiers in immunology · 2018Review
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Rhesus (rh) but not human (hu) TRIM5α potently restricts human immunodeficiency virus (HIV)-1 infection. It is not clear why huTRIM5α fails to effectively block HIV infection, but it is thought to have a lower affinity for the viral core. Using primary human CD4 T cells, we investigated the ability of huTRIM5α, rhTRIM5α, and the huTRIM5αR323-332 B30.2/SPRY patch-mutant to form cytoplasmic bodies, postulated as key components of the HIV-1 restriction apparatus. Both rhTRIM5α and huTRIM5αR323-332 formed pronounced cytoplasmic bodies, whereas cytoplasmic bodies in T cells overexpressing huTRIM5α were present but more difficult to detect. As expression of all three TRIM5α orthologs was similar at the RNA level, we next investigated the role of protein stability in conferring TRIM5α-mediated HIV-1 restriction. Both steady-state and pulse-chase experiments revealed that the huTRIM5α protein was much less stable than rhTRIM5α, and this difference correlated with higher self-ubiquitination activity. Using a stabilized form of huTRIM5α in which the steady-state expression level was more similar to rhTRIM5α, we observed comparable HIV-1 restriction activity in multi-round HIV-1 challenge assays. Lastly, primary human CD4 T cells expressing a stabilized huTRIM5α were protected from HIV-1-mediated destruction in vivo, indicating that efforts to stabilize huTRIM5α should have significant long-term therapeutic value.
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