ArticleProceedings of the National Academy of Sciences of the United States of America2008
Cytidine deamination induced HIV-1 drug resistance.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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.
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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.
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Who cites it
104 citing papers in PubMed.
- Understanding Basic Concepts of Viral Quasispecies: From Evolutionary Dynamics to Clinical Relevance.Pathogens (Basel, Switzerland) · 2026Review
- Limitations of inferring antiviral efficacy of interfering particles from observational natural histories.bioRxiv : the preprint server for biology · 2026Article
- Single-cell delineation of strain-specific HIV-1 Vif activities using dual reporter sensor cells and live cell imaging.Journal of virology · 2025Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- HIV-1 Vif global diversity and possible APOBEC-mediated response since 1980.Virus evolution · 2025Article
- Article
- Review
- Inverted repeats in the monkeypox virus genome are hot spots for mutation.Journal of medical virology · 2023Article
- Consistency of drug-resistant mutations in plasma and peripheral blood mononuclear cells of patients with treatment-naïve and treatment-experienced HIV-1 infection.Frontiers in cellular and infection microbiology · 2023Article
- The current toolbox for APOBEC drug discovery.Trends in pharmacological sciences · 2022Review
- 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
- Molecular Biology and Diversification of Human Retroviruses.Frontiers in virology (Lausanne, Switzerland) · 2022Article
- Human APOBEC3 Variations and Viral Infection.Viruses · 2021Review
- Examination of the APOBEC3 Barrier to Cross Species Transmission of Primate Lentiviruses.Viruses · 2021Review
- Influenza virus repurposes the antiviral protein IFIT2 to promote translation of viral mRNAs.Nature microbiology · 2020Article
- Review
- Antagonism of PP2A is an independent and conserved function of HIV-1 Vif and causes cell cycle arrest.eLife · 2020Article
- Long-Acting Rilpivirine (RPV) Preexposure Prophylaxis Does Not Inhibit Vaginal Transmission of RPV-Resistant HIV-1 or Select for High-Frequency Drug Resistance in Humanized Mice.Journal of virology · 2020Article
- Impact of Suboptimal APOBEC3G Neutralization on the Emergence of HIV Drug Resistance in Humanized Mice.Journal of virology · 2020Article
- USP49 potently stabilizes APOBEC3G protein by removing ubiquitin and inhibits HIV-1 replication.eLife · 2019Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The HIV-1 Vif protein is essential for overcoming the antiviral activity of DNA-editing apolipoprotein B mRNA editing enzyme, catalytic polypeptide 3 (APOBEC3) cytidine deaminases. We show that naturally occurring HIV-1 Vif point mutants with suboptimal anti-APOBEC3G activity induce the appearance of proviruses with lamivudine (3TC) drug resistance-associated mutations before any drug exposure. These mutations, ensuing from cytidine deamination events, were detected in >40% of proviruses with partially defective Vif mutants. Transfer of drug resistance from hypermutated proviruses via recombination allowed for 3TC escape under culture conditions prohibitive for any WT viral growth. These results demonstrate that defective hypermutated genomes can shape the phenotype of the circulating viral population. Partially active Vif alleles resulting in incomplete neutralization of cytoplasmic APOBEC3 molecules are directly responsible for the generation of a highly diverse, yet G-to-A biased, proviral reservoir, which can be exploited by HIV-1 to generate viable and drug-resistant progenies.
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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.