ArticleProceedings of the National Academy of Sciences of the United States of America2006
The Vif and Vpr accessory proteins independently cause HIV-1-induced T cell cytopathicity and cell cycle arrest.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.
- HIV Genome-Wide Protein Associations: a Review of 30 Years of Research.Microbiology and molecular biology reviews : MMBR · 2016Pooled it
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- Article
- Elimination of Human Immunodeficiency Virus Reservoirs Harboring Intact Proviruses.The Journal of infectious diseases · 2026Article
- HIV-1 Vif and Vpr cooperatively modulate the cell cycle to maximize per-cell virion production.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Transcription factor BACH2 shapes tissue-resident memory T cell programs to promote HIV-1 persistence.Immunity · 2025Article
- APOBEC3 and the mutational signature of lentiviral vectors.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- In vitro HIV DNA integration in STAT3 drives T cell persistence-A model of HIV-associated T cell lymphoma.PLoS pathogens · 2025Article
- HIV Vpr activates a nucleolar-specific ATR pathway to degrade the nucleolar stress sensor CCDC137.Nucleic acids research · 2025Article
- Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- Central Memory CD4 T Cells from Persons with HIV Accumulate DNA Content Defects During Proliferative Response.AIDS research and human retroviruses · 2025Article
- Identification of polymorphisms associated with attenuation of Vif and Vpr in HIV-1 Elite Controllers.Memorias do Instituto Oswaldo Cruz · 2025Article
- HIV-1 Vif disrupts phosphatase feedback regulation at the kinetochore, leading to a pronounced pseudo-metaphase arrest.bioRxiv : the preprint server for biology · 2024Article
- Structural insights into PPP2R5A degradation by HIV-1 Vif.Nature structural & molecular biology · 2024Article
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- HIV Expression in Infected T Cell Clones.Viruses · 2024Review
- Transcriptomic study reveals changes of lncRNAs in PBMCs from HIV-1 patients before and after ART.Scientific reports · 2023Article
- Rev-Rev Response Element Activity Selection Bias at the Human Immunodeficiency Virus Transmission Bottleneck.Open forum infectious diseases · 2023Article
- Article
29 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
HIV type I (HIV-1) can cause G(2) cell cycle arrest and death of CD4(+) T lymphocytes in vitro and inexorable depletion of these cells in vivo. However, the molecular mechanism of viral cytopathicity has not been satisfactorily elucidated. Previously, we showed that HIV-1 kills T cells by a necrotic form of cell death that requires high level expression of an integrated provirus but not the env or nef genes. To determine which viral protein(s) are required for cell death, we systematically mutated, alone and in combination, the ORFs of the NL4-3 strain of HIV-1. We found that the elimination of the viral functions encoded by gag-pol and vpu, tat, and rev did not mitigate cytopathicity. However, elimination of the vif and vpr accessory genes together, but not individually, renders the virus incapable of causing cell death and G(2) cell cycle blockade. We thus identify vif and vpr as necessary for T cell cytopathic effects induced by HIV-1. These findings may provide an important insight into the molecular mechanism of viral pathogenesis in AIDS.
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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.