ArticlePLoS genetics2012
APOBEC3G-induced hypermutation of human immunodeficiency virus type-1 is typically a discrete "all or nothing" phenomenon.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Switching to bictegravir/emtricitabine/tenofovir alafenamide maintained HIV-1 RNA suppression in participants with archived antiretroviral resistance including M184V/I.The Journal of antimicrobial chemotherapy · 2019Trial
- How should APOBEC3-induced resistance mutations be considered in the management of antiretroviral therapy?The Journal of antimicrobial chemotherapy · 2025Article
- A simple phylogenetic approach to analyze hypermutated HIV proviruses reveals insights into their dynamics and persistence during antiretroviral therapy.Virus evolution · 2025Article
- HIV-1 Vif global diversity and possible APOBEC-mediated response since 1980.Virus evolution · 2025Article
- Learning From Full Characterization of HIV Proviruses in People Receiving Long-Acting Cabotegravir/Rilpivirine With a History of Replication on the Antiretroviral Classes.Open forum infectious diseases · 2025Article
- Use of genotypic HIV DNA testing: a DELPHI-type consensus.The Journal of antimicrobial chemotherapy · 2024Article
- Article
- Recent advances in CD8Heliyon · 2023Review
- SARS-CoV-2 Evolution: On the Sudden Appearance of the Omicron Variant.Journal of virology · 2022Article
- Article
- PCIP-seq: simultaneous sequencing of integrated viral genomes and their insertion sites with long reads.Genome biology · 2021Article
- Foamy Viruses, Bet, and APOBEC3 Restriction.Viruses · 2021Review
- Review
- Impact of Suboptimal APOBEC3G Neutralization on the Emergence of HIV Drug Resistance in Humanized Mice.Journal of virology · 2020Article
- From APOBEC to ZAP: Diverse mechanisms used by cellular restriction factors to inhibit virus infections.Biochimica et biophysica acta. Molecular cell research · 2019Review
- HIV-1 Infection and Type 1 Interferon: Navigating Through Uncertain Waters.AIDS research and human retroviruses · 2019Review
- A New Class of Antiretroviral Enabling Innate Immunity by Protecting APOBEC3 from HIV Vif-Dependent Degradation.Trends in molecular medicine · 2018Review
- APOBEC3G Regulation of the Evolutionary Race Between Adaptive Immunity and Viral Immune Escape Is Deeply Imprinted in the HIV Genome.Frontiers in immunology · 2018Article
- Post-translational Modification-Based Regulation of HIV Replication.Frontiers in microbiology · 2018Review
- HIV-1 tolerates changes in A-count in a small segment of the pol gene.Retrovirology · 2017Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The rapid evolution of Human Immunodeficiency Virus (HIV-1) allows studies of ongoing host-pathogen interactions. One key selective host factor is APOBEC3G (hA3G) that can cause extensive and inactivating Guanosine-to-Adenosine (G-to-A) mutation on HIV plus-strand DNA (termed hypermutation). HIV can inhibit this innate anti-viral defense through binding of the viral protein Vif to hA3G, but binding efficiency varies and hypermutation frequencies fluctuate in patients. A pivotal question is whether hA3G-induced G-to-A mutation is always lethal to the virus or if it may occur at sub-lethal frequencies that could increase viral diversification. We show in vitro that limiting-levels of hA3G-activity (i.e. when only a single hA3G-unit is likely to act on HIV) produce hypermutation frequencies similar to those in patients and demonstrate in silico that potentially non-lethal G-to-A mutation rates are ∼10-fold lower than the lowest observed hypermutation levels in vitro and in vivo. Our results suggest that even a single incorporated hA3G-unit is likely to cause extensive and inactivating levels of HIV hypermutation and that hypermutation therefore is typically a discrete "all or nothing" phenomenon. Thus, therapeutic measures that inhibit the interaction between Vif and hA3G will likely not increase virus diversification but expand the fraction of hypermutated proviruses within the infected host.
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