ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2009
APOBEC proteins and intrinsic resistance to HIV-1 infection.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 2 of them syntheses 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
187 citing papers in PubMed, 2 syntheses or guidelines pooled it, 273 citations in OpenAlex.
- Disrupting Mechanisms that Regulate Genomic Repeat Elements to Combat Cancer and Drug Resistance.Frontiers in cell and developmental biology · 2022Pooled it
- Identifying potential survival strategies of HIV-1 through virus-host protein interaction networks.BMC systems biology · 2010Pooled it
- HIV-1 APOBEC-context Mutations Detected by Next-Generation Sequencing in Plasma: Implications for Drug Resistance Interpretation.The Journal of infectious diseases · 2026Article
- The Implications of HIV-1 Subtypes on Pathogenesis, Reservoirs and Cure Strategies.Current HIV/AIDS reports · 2026Review
- Article
- Article
- Article
- Novel drug targets for monkeypox: From viral to host proteins.Infectious medicine · 2025Article
- 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
- Next-Generation Sequencing Methods to Determine the Accuracy of Retroviral Reverse Transcriptases: Advantages and Limitations.Viruses · 2025Review
- HIV-1 Vif global diversity and possible APOBEC-mediated response since 1980.Virus evolution · 2025Article
- C→U transition biases in SARS-CoV-2: still rampant 4 years from the start of the COVID-19 pandemic.mBio · 2024Article
- Review
- Review
- Review
- The Disassociation of A3G-Related HIV-1 cDNA G-to-A Hypermutation to Viral Infectivity.Viruses · 2024Article
- Vulnerability to APOBEC3G linked to the pathogenicity of deltaretroviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The timing of HIV-1 infection of cells that persist on therapy is not strongly influenced by replication competency or cellular tropism of the provirus.PLoS pathogens · 2024Article
- Innate immune responses reverse HIV cognitive disease in mice: Profile by RNAseq in the brain.Virology · 2024Article
- Comparative physiological anthropogeny: exploring molecular underpinnings of distinctly human phenotypes.Physiological reviews · 2023Review
127 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
1 author at 1 institution in 2 countries.
Funding
Abstract
Members of the APOBEC family of cellular polynucleotide cytidine deaminases, most notably APOBEC3G and APOBEC3F, are potent inhibitors of HIV-1 infection. Wild type HIV-1 infections are largely spared from APOBEC3G/F function through the action of the essential viral protein, Vif. In the absence of Vif, APOBEC3G/F are encapsidated by budding virus particles leading to excessive cytidine (C) to uridine (U) editing of negative sense reverse transcripts in newly infected cells. This registers as guanosine (G) to adenosine (A) hypermutations in plus-stranded cDNA. In addition to this profoundly debilitating effect on genetic integrity, APOBEC3G/F also appear to inhibit viral DNA synthesis by impeding the translocation of reverse transcriptase along template RNA. Because the functions of Vif and APOBEC3G/F proteins oppose each other, it is likely that fluctuations in the Vif-APOBEC balance may influence the natural history of HIV-1 infection, as well as viral sequence diversification and evolution. Given Vif's critical role in suppressing APOBEC3G/F function, it can be argued that pharmacologic strategies aimed at restoring the activity of these intrinsic anti-viral factors in the context of infected cells in vivo have clear therapeutic merit, and therefore deserve aggressive pursuit.
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.