ReviewExperimental and molecular pathology2008
HIV-1 Vpr: mechanisms of G2 arrest and apoptosis.
Review in Experimental and molecular pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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
67 citing papers in PubMed, 106 citations in OpenAlex.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- Blocking Host Factors IAP and DDX3 Activates HIV-1 Transcription and Increases Apoptosis Sensitivity of HIV-1 Infected Cells.Pathogens (Basel, Switzerland) · 2026Article
- Review
- Investigating the Potential Role of Capsaicin in Facilitating the Spread of Coxsackievirus B3 via Extracellular Vesicles.International journal of molecular sciences · 2026Article
- HIV-Induced Apoptosis: Host Defense and Viral Strategy.Biology · 2025Review
- In Situ Vaccination with a Vpr-Derived Peptide Elicits Systemic Antitumor Immunity by Improving Tumor Immunogenicity.Vaccines · 2025Article
- The HIV-1Viruses · 2024Article
- Vpr driving DNA methylation variation of CD4 + T cells in HIV-1 infection.Virology journal · 2024Article
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- HIV/Mtb Co-Infection: From the Amplification of Disease Pathogenesis to an "Emerging Syndemic".Microorganisms · 2023Review
- SMAC Mimetics as Therapeutic Agents in HIV Infection.Frontiers in immunology · 2021Review
- Article
- Immune escape mutations in HIV-1 controllers in the Brazilian Amazon region.BMC infectious diseases · 2020Article
- Insights into the Gene Expression Profiles of Active and Restricted Red/Green-HIVJournal of virology · 2020Article
- Dual Functionality of HIV-1 Vif in APOBEC3 Counteraction and Cell Cycle Arrest.Frontiers in microbiology · 2020Review
- TIGIT Blockade: A Multipronged Approach to Target the HIV Reservoir.Frontiers in cellular and infection microbiology · 2020Review
- Review
- Potential of the NKG2D/NKG2DL Axis in NK Cell-Mediated Clearance of the HIV-1 Reservoir.International journal of molecular sciences · 2019Review
- The DNA deaminase APOBEC3B interacts with the cell-cycle protein CDK4 and disrupts CDK4-mediated nuclear import of Cyclin D1.The Journal of biological chemistry · 2019Article
- HIV-1 Vpr counteracts HLTF-mediated restriction of HIV-1 infection in T cells.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
7 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 3 institutions in 2 countries.
Funding
Abstract
Since the first isolation of HIV-1 from a patient with generalized lymphadenopathy in 1983, great progress has been made in understanding the viral life cycle and the functional nuances of each of the nine genes encoded by HIV-1. Considerable attention has been paid to four small HIV-1 open reading frames, vif, vpr, vpu and nef. These genes were originally termed "accessory" because their deletion failed to completely disable viral replication in vitro. More than twenty years after the cloning and sequencing of HIV-1, a great deal of information is available regarding the multiple functions of the accessory proteins and it is well accepted that, collectively, these gene products modulate the host cell biology to favor viral replication, and that they are largely responsible for the pathogenesis of HIV-1. Expression of Vpr, in particular, leads to cell cycle arrest in G(2), followed by apoptosis. Here we summarize our current understanding of Vpr biology with a focus on Vpr-induced G(2) arrest and apoptosis.
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.