ArticleBlood2011
HIV-1 Vif promotes the G₁- to S-phase cell-cycle transition.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 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
- Identification of Virus-Host Interactions.Advances in experimental medicine and biology · 2026Review
- Article
- Contrasting Effect of Curcumin on Hepatitis B Virus Replication According to the Hepatoma Cell Line.Pathogens (Basel, Switzerland) · 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
- Are BET Inhibitors yet Promising Latency-Reversing Agents for HIV-1 Reactivation in AIDS Therapy?Viruses · 2021Review
- Article
- A computational analysis of transcriptional profiles from CD8(+) T lymphocytes reveals potential mechanisms of HIV/AIDS control and progression.Computational and structural biotechnology journal · 2021Article
- Review
- Intertwined: SAMHD1 cellular functions, restriction, and viral evasion strategies.Medical microbiology and immunology · 2019Review
- Cell Size-Based Decision-Making of a Viral Gene Circuit.Cell reports · 2018Article
- Hepatitis B Virus Deregulates the Cell Cycle To Promote Viral Replication and a Premalignant Phenotype.Journal of virology · 2018Article
- HIV-1 Vif's Capacity To Manipulate the Cell Cycle Is Species Specific.Journal of virology · 2018Article
- The role of cullin 5-containing ubiquitin ligases.Cell division · 2016Review
- Evolutionarily conserved pressure for the existence of distinct G2/M cell cycle arrest and A3H inactivation functions in HIV-1 Vif.Cell cycle (Georgetown, Tex.) · 2015Article
- Activation of HIV-1 from latent infection via synergy of RUNX1 inhibitor Ro5-3335 and SAHA.PLoS pathogens · 2014Article
- Gene expression profiling of CD4⁺ T cells in treatment-naive HIV, HCV mono- or co-infected Chinese.Virology journal · 2014Article
- Visualizing Vpr-induced G2 arrest and apoptosis.PloS one · 2014Article
- Suppression of APOBEC3-mediated restriction of HIV-1 by Vif.Frontiers in microbiology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
HIV-1 depends on host-cell resources for replication, access to which may be limited to a particular phase of the cell cycle. The HIV-encoded proteins Vpr (viral protein R) and Vif (viral infectivity factor) arrest cells in the G₂ phase; however, alteration of other cell-cycle phases has not been reported. We show that Vif drives cells out of G₁ and into the S phase. The effect of Vif on the G₁- to-S transition is distinct from its effect on G₂, because G₂ arrest is Cullin5-dependent, whereas the G₁- to-S progression is Cullin5-independent. Using mass spectrometry, we identified 2 novel cellular partners of Vif, Brd4 and Cdk9, both of which are known to regulate cell-cycle progression. We confirmed the interaction of Vif and Cdk9 by immunoprecipitation and Western blot, and showed that small interfering RNAs (siRNAs) specific for Cdk9 inhibit the Vif-mediated G₁- to-S transition. These data suggest that Vif regulates early cell-cycle progression, with implications for infection and latency.
Indexed as
Identifiers
What OpenQuestion holds
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.