ArticleRetrovirology2007
The dimerization domain of HIV-1 viral infectivity factor Vif is required to block virion incorporation of APOBEC3G.
Article in Retrovirology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- Design of Vif-Derived Peptide Inhibitors with Anti-HIV-1 Activity by Interrupting Vif-CBFβ Interaction.Viruses · 2024Article
- Leveraging the therapeutic, biological, and self-assembling potential of peptides for the treatment of viral infections.Journal of controlled release : official journal of the Controlled Release Society · 2022Review
- Amide Bond Bioisosteres: Strategies, Synthesis, and Successes.Journal of medicinal chemistry · 2020Review
- A New Class of Antiretroviral Enabling Innate Immunity by Protecting APOBEC3 from HIV Vif-Dependent Degradation.Trends in molecular medicine · 2018Review
- An analog of camptothecin inactive against Topoisomerase I is broadly neutralizing of HIV-1 through inhibition of Vif-dependent APOBEC3G degradation.Antiviral research · 2016Article
- Anti-APOBEC3G activity of HIV-1 Vif protein is attenuated in elite controllers.Journal of virology · 2015Article
- Determinants of efficient degradation of APOBEC3 restriction factors by HIV-1 Vif.Journal of virology · 2014Article
- Structural insights for HIV-1 therapeutic strategies targeting Vif.Trends in biochemical sciences · 2014Review
- High-affinity recognition of HIV-1 frameshift-stimulating RNA alters frameshifting in vitro and interferes with HIV-1 infectivity.Journal of medicinal chemistry · 2014Article
- Structural analysis of viral infectivity factor of HIV type 1 and its interaction with A3G, EloC and EloB.PloS one · 2014Article
- Mapping the Vif-A3G interaction using peptide arrays: a basis for anti-HIV lead peptides.Bioorganic & medicinal chemistry · 2013Article
- APOBEC3G impairs the multimerization of the HIV-1 Vif protein in living cells.Journal of virology · 2013Article
- HIV-1 viral infectivity factor (Vif) alters processive single-stranded DNA scanning of the retroviral restriction factor APOBEC3G.The Journal of biological chemistry · 2013Article
- Development of a robust cell-based high-throughput screening assay to identify targets of HIV-1 viral protein R dimerization.Drug design, development and therapy · 2013Article
- APOBEC3G-Augmented Stem Cell Therapy to Modulate HIV Replication: A Computational Study.PloS one · 2013Article
- Host restriction factors in retroviral infection: promises in virus-host interaction.Retrovirology · 2012Review
- APOBEC3G expression and hypermutation are inversely associated with human immunodeficiency virus type 1 (HIV-1) burden in vivo.Virology · 2012Article
- Small-molecule inhibition of human immunodeficiency virus type 1 replication by targeting the interaction between Vif and ElonginC.Journal of virology · 2012Article
- Protein intrinsic disorder as a flexible armor and a weapon of HIV-1.Cellular and molecular life sciences : CMLS · 2012Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe HIV-1 accessory protein known as viral infectivity factor or Vif binds to the host defence factor human APOBEC3G (hA3G) and prevents its assembly with viral particles and mediates its elimination through ubiquitination and degradation by the proteosomal pathway. In the absence of Vif, hA3G becomes incorporated within viral particles. During the post entry phase of infection, hA3G attenuates viral replication by binding to the viral RNA genome and deaminating deoxycytidines to form deoxyuridines within single stranded DNA regions of the replicated viral genome. Vif dimerization has been reported to be essential for viral infectivity but the mechanistic requirement for Vif multimerization is unknown.
resultsWe demonstrate that a peptide antagonist of Vif dimerization fused to the cell transduction domain of HIV TAT suppresses live HIV-1 infectivity. We show rapid cellular uptake of the peptide and cytoplasmic distribution. Robust suppression of viral infectivity was dependent on the expression of Vif and hA3G. Disruption of Vif multimerization resulted in the production of virions with markedly increased hA3G content and reduced infectivity.
conclusionThe role of Vif multimerization in viral infectivity of nonpermissive cells has been validated with an antagonist of Vif dimerization. An important part of the mechanism for this antiretroviral effect is that blocking Vif dimerization enables hA3G incorporation within virions. We propose that Vif multimers are required to interact with hA3G to exclude it from viral particles during their assembly. Blocking Vif dimerization is an effective means of sustaining hA3G antiretroviral activity in HIV-1 infected cells. Vif dimerization is therefore a validated target for therapeutic HIV-1/AIDS drug development.
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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.