ReviewRetrovirology2008
HIV-1 Vif, APOBEC, and intrinsic immunity.
Review in Retrovirology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 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
213 citing papers in PubMed.
- Lack of association between intact/deletion polymorphisms of the APOBEC3B gene and HIV-1 risk.PloS one · 2014Trial
- Anelloviruses: From General Biology to Their Role as Biomarkers of Immune Competence in HIV Infection.Viruses · 2026Review
- Review
- Human microRNA miR-197-3p positively regulates HIV-1 virion infectivity through its target DDX52 by stabilizing Vif protein expression.The Journal of biological chemistry · 2025Article
- Review
- The roles of DNA damage repair and innate immune surveillance pathways in HPV pathogenesis.Virology · 2024Review
- Distinguishing preferences of human APOBEC3A and APOBEC3B for cytosines in hairpin loops, and reflection of these preferences in APOBEC-signature cancer genome mutations.Nature communications · 2024Article
- Human endogenous retroviruses and exogenous viral infections.Frontiers in cellular and infection microbiology · 2024Review
- Interactions between HIV proteins and host restriction factors: implications for potential therapeutic intervention in HIV infection.Frontiers in immunology · 2024Review
- Evidence Supporting That C-to-U RNA Editing Is the Major Force That Drives SARS-CoV-2 Evolution.Journal of molecular evolution · 2023Article
- Article
- Epigenetic Abnormalities in Chondrosarcoma.International journal of molecular sciences · 2023Review
- Article
- APOBEC3G expression correlates with unfavorable prognosis and immune infiltration in kidney renal clear cell carcinoma.Heliyon · 2022Article
- The current toolbox for APOBEC drug discovery.Trends in pharmacological sciences · 2022Review
- Unwinding the roles of RNA helicase MOV10.Wiley interdisciplinary reviews. RNA · 2022Review
- Two different kinds of interaction modes of deaminase APOBEC3A with single-stranded DNA in solution detected by nuclear magnetic resonance.Protein science : a publication of the Protein Society · 2022Article
- Human Immunodeficiency Virus Type 1 Vif Up-Regulates the Expression of TatFrontiers in microbiology · 2022Article
- APOBEC3 selects V179I in HIV-1 reverse transcriptase to provide selective advantage for non-nucleoside reverse transcriptase inhibitor-resistant mutants.Frontiers in virology (Lausanne, Switzerland) · 2022Article
- APOBEC3B Potently Restricts HIV-2 but Not HIV-1 in a Vif-Dependent Manner.Journal of virology · 2021Article
153 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
2 authors.
Funding
Abstract
Members of the APOBEC family of cellular cytidine deaminases represent a recently identified group of proteins that provide immunity to infection by retroviruses and protect the cell from endogenous mobile retroelements. Yet, HIV-1 is largely immune to the intrinsic antiviral effects of APOBEC proteins because it encodes Vif (viral infectivity factor), an accessory protein that is critical for in vivo replication of HIV-1. In the absence of Vif, APOBEC proteins are encapsidated by budding virus particles and either cause extensive cytidine to uridine editing of negative sense single-stranded DNA during reverse transcription or restrict virus replication through deaminase-independent mechanisms. Thus, the primary function of Vif is to prevent encapsidation of APOBEC proteins into viral particles. This is in part accomplished by the ability of Vif to induce the ubiquitin-dependent degradation of some of the APOBEC proteins. However, Vif is also able to prevent encapsidation of APOBEC3G and APOBEC3F through degradation-independent mechanism(s). The goal of this review is to recapitulate current knowledge of the functional interaction of HIV-1 and its Vif protein with the APOBEC3 subfamily of proteins and to summarize our present understanding of the mechanism of APOBEC3-dependent retrovirus restriction.
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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.