ArticleCurrent biology : CB2008
Evolution of HIV-1 isolates that use a novel Vif-independent mechanism to resist restriction by human APOBEC3G.
Article in Current biology : CB, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- Article
- APOBEC3 degradation is the primary function of HIV-1 Vif for virus replication in the myeloid cell line THP-1.bioRxiv : the preprint server for biology · 2023Article
- Examination of the APOBEC3 Barrier to Cross Species Transmission of Primate Lentiviruses.Viruses · 2021Review
- Specific Deubiquitinating Enzymes Promote Host Restriction Factors Against HIV/SIV Viruses.Frontiers in immunology · 2021Article
- Characterization of an A3G-VifMolecular & cellular proteomics : MCP · 2021Article
- Potential Utilization of APOBEC3-Mediated Mutagenesis for an HIV-1 Functional Cure.Frontiers in microbiology · 2021Review
- The Role of RNA in HIV-1 Vif-Mediated Degradation of APOBEC3H.Journal of molecular biology · 2019Article
- Structural basis of antagonism of human APOBEC3F by HIV-1 Vif.Nature structural & molecular biology · 2019Article
- HIV-1 restriction by endogenous APOBEC3G in the myeloid cell line THP-1.The Journal of general virology · 2019Article
- Article
- Natural APOBEC3C variants can elicit differential HIV-1 restriction activity.Retrovirology · 2018Article
- Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease.Nature communications · 2018Article
- Simian Immunodeficiency Virus Vif and Human APOBEC3B Interactions Resemble Those between HIV-1 Vif and Human APOBEC3G.Journal of virology · 2018Article
- HIV-1 adaptation studies reveal a novel Env-mediated homeostasis mechanism for evading lethal hypermutation by APOBEC3G.PLoS pathogens · 2018Article
- Evaluation of sequence variability in HIV-1 gp41 C-peptide helix-grafted proteins.Bioorganic & medicinal chemistry · 2018Article
- The Antiviral and Cancer Genomic DNA Deaminase APOBEC3H Is Regulated by an RNA-Mediated Dimerization Mechanism.Molecular cell · 2018Article
- HIV-1 competition experiments in humanized mice show that APOBEC3H imposes selective pressure and promotes virus adaptation.PLoS pathogens · 2017Article
- Long-term passage of Vif-null HIV-1 in CD4Virology · 2017Article
- Core Binding Factor β Protects HIV, Type 1 Accessory Protein Viral Infectivity Factor from MDM2-mediated Degradation.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The human APOBEC3G protein restricts the replication of Vif-deficient HIV-1 by deaminating nascent viral cDNA cytosines to uracils, leading to viral genomic strand G-to-A hypermutations. However, the HIV-1 Vif protein triggers APOBEC3G degradation, which helps to explain why this innate defense does not protect patients. The APOBEC3G-Vif interaction is a promising therapeutic target, but the benefit of the enabling of HIV-1 restriction in patients is unlikely to be known until Vif antagonists are developed. As a necessary prelude to such studies, cell-based HIV-1 evolution experiments were done to find out whether APOBEC3G can provide a long-term block to Vif-deficient virus replication and, if so, whether HIV-1 variants that resist restriction would emerge. APOBEC3G-expressing T cells were infected with Vif-deficient HIV-1. Virus infectivity was suppressed in 45/48 cultures for more than five weeks, but replication was eventually detected in three cultures. Virus-growth characteristics and sequencing demonstrated that these isolates were still Vif-deficient and that in fact, these viruses had acquired a promoter mutation and a Vpr null mutation. Resistance occurred by a novel tolerance mechanism in which the resistant viruses packaged less APOBEC3G and accumulated fewer hypermutations. These data support the development of antiretrovirals that antagonize Vif and thereby enable endogenous APOBEC3G to suppress HIV-1 replication.
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