ArticleJournal of molecular biology2011
Multifaceted counter-APOBEC3G mechanisms employed by HIV-1 Vif.
Article in Journal of molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- The Disassociation of A3G-Related HIV-1 cDNA G-to-A Hypermutation to Viral Infectivity.Viruses · 2024Article
- Direct inhibition of human APOBEC3 deaminases by HIV-1 Vif independent of the proteolysis pathway.Biophysical journal · 2024Article
- Host-mediated RNA editing in viruses.Biology direct · 2023Review
- Aromatic disulfides as potential inhibitors against interaction between deaminase APOBEC3G and HIV infectivity factor.Acta biochimica et biophysica Sinica · 2022Article
- APOBEC3B Potently Restricts HIV-2 but Not HIV-1 in a Vif-Dependent Manner.Journal of virology · 2021Article
- APOBEC3F Constitutes a Barrier to Successful Cross-Species Transmission of Simian Immunodeficiency Virus SIVsmm to Humans.Journal of virology · 2021Article
- Multifaceted HIV-1 Vif interactions with human E3 ubiquitin ligase and APOBEC3s.The FEBS journal · 2021Article
- Review
- Foamy Viruses, Bet, and APOBEC3 Restriction.Viruses · 2021Review
- Characterization of an A3G-VifMolecular & cellular proteomics : MCP · 2021Article
- Structural basis of antagonism of human APOBEC3F by HIV-1 Vif.Nature structural & molecular biology · 2019Article
- Article
- APOBEC Enzymes as Targets for Virus and Cancer Therapy.Cell chemical biology · 2018Review
- Reassessing APOBEC3G Inhibition by HIV-1 Vif-Derived Peptides.Journal of molecular biology · 2017Article
- APOBEC3G and APOBEC3F Act in Concert To Extinguish HIV-1 Replication.Journal of virology · 2016Article
- Inhibition of APOBEC3G activity impedes double-stranded DNA repair.The FEBS journal · 2016Article
- Zinc enhancement of cytidine deaminase activity highlights a potential allosteric role of loop-3 in regulating APOBEC3 enzymes.Scientific reports · 2015Article
- APOBEC3G Interacts with ssDNA by Two Modes: AFM Studies.Scientific reports · 2015Article
- Determinants of efficient degradation of APOBEC3 restriction factors by HIV-1 Vif.Journal of virology · 2014Article
- HIV-1 Vif inhibits G to A hypermutations catalyzed by virus-encapsidated APOBEC3G to maintain HIV-1 infectivity.Retrovirology · 2014Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
In the absence of human immunodeficiency virus type 1 (HIV-1) Vif protein, the host antiviral deaminase apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (A3G) restricts the production of infectious HIV-1 by deamination of dC residues in the negative single-stranded DNA produced by reverse transcription. The Vif protein averts the lethal threat of deamination by precluding the packaging of A3G into assembling virions by mediating proteasomal degradation of A3G. In spite of this robust Vif activity, residual A3G molecules that escape degradation and incorporate into newly assembled virions are potentially deleterious to the virus. We hypothesized that virion-associated Vif inhibits A3G enzymatic activity and therefore prevents lethal mutagenesis of the newly synthesized viral DNA. Here, we show that (i) Vif-proficient HIV-1 particles released from H9 cells contain A3G with lower specific activity compared with Δvif-virus-associated A3G, (ii) encapsidated HIV-1 Vif inhibits the deamination activity of recombinant A3G, and (iii) purified HIV-1 Vif protein and the Vif-derived peptide Vif25-39 inhibit A3G activity in vitro at nanomolar concentrations in an uncompetitive manner. Our results manifest the potentiality of Vif to control the deamination threat in virions or in the pre-integration complexes following entry to target cells. Hence, virion-associated Vif could serve as a last line of defense, protecting the virus against A3G antiviral activity.
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Registered trials
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