ArticleThe Journal of biological chemistry2010
Differential anti-APOBEC3G activity of HIV-1 Vif proteins derived from different subtypes.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 61 citations in OpenAlex.
- Strain-specific epistasis shapes fitness landscapes of APOBEC3G antagonism by HIV-1 Vif proteins.Science advances · 2026Article
- Long-read deep sequencing reveals high rates of multilineage transmission and rapid viral population changes in acute HIV infection.Nature communications · 2026Article
- Article
- Fitness Landscapes of APOBEC3G Antagonism by HIV-1 Vif proteins.bioRxiv : the preprint server for biology · 2025Article
- Single-cell delineation of strain-specific HIV-1 Vif activities using dual reporter sensor cells and live cell imaging.Journal of virology · 2025Article
- HIV-1 Vif global diversity and possible APOBEC-mediated response since 1980.Virus evolution · 2025Article
- The association between HIV-1 Tat and Vif amino acid sequence variation, inflammation and Trp-Kyn metabolism: an exploratory investigation.BMC infectious diseases · 2024Article
- HIV-1 Vif protein sequence variations in South African people living with HIV and their influence on Vif-APOBEC3G interaction.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024Article
- APOBEC3B Potently Restricts HIV-2 but Not HIV-1 in a Vif-Dependent Manner.Journal of virology · 2021Article
- SARS-CoV-2 D614G spike mutation increases entry efficiency with enhanced ACE2-binding affinity.Nature communications · 2021Article
- Differential Vpu-Mediated CD4 and Tetherin Downregulation Functions among Major HIV-1 Group M Subtypes.Journal of virology · 2020Article
- Antagonism of PP2A is an independent and conserved function of HIV-1 Vif and causes cell cycle arrest.eLife · 2020Article
- Understanding the mechanisms driving the spread of subtype C HIV-1.EBioMedicine · 2020Review
- Expression Level of HIV-1 Vif Can Be Fluctuated by Natural Nucleotide Variations in theFrontiers in microbiology · 2019Article
- Patterns of genomic site inheritance in HIV-1M inter-subtype recombinants delineate the most likely genomic sites of subtype-specific adaptation.Virus evolution · 2018Article
- Single-Strand Consensus Sequencing Reveals that HIV Type but not Subtype Significantly Impacts Viral Mutation Frequencies and Spectra.Journal of molecular biology · 2017Article
- Subtype-Specific Differences in Gag-Protease-Driven Replication Capacity Are Consistent with Intersubtype Differences in HIV-1 Disease Progression.Journal of virology · 2017Article
- In vitro functional assessment of natural HIV-1 group M Vpu sequences using a universal priming approach.Journal of virological methods · 2017Article
- Rev-RRE Functional Activity Differs Substantially Among Primary HIV-1 Isolates.AIDS research and human retroviruses · 2016Article
- Functional characterization of Vif proteins from HIV-1 infected patients with different APOBEC3G haplotypes.AIDS (London, England) · 2016Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antiretroviral cytidine deaminase APOBEC3G, which is abundantly expressed in peripheral blood lymphocytes and macrophages, strongly protects these cells against HIV-1 infection. The HIV-1 Vif protein overcomes this antiviral effect by enhancing proteasome-mediated APOBEC3G degradation and is key for maintaining viral infectivity. The 579-bp-long vif gene displays high genetic diversity among HIV-1 subtypes. Therefore, it is intriguing to address whether Vif proteins derived from different subtypes differ in their viral defense activity against APOBEC3G. Expression plasmids encoding Vif proteins derived from subtypes A, B, C, CRF01_AE, and CRF02_AG isolates were created, and their anti-APOBEC3G activities were compared. Viruses produced from cells expressing APOBEC3G and Vif proteins from different subtypes showed relatively different viral infectivities. Notably, subtype C-derived Vif proteins tested had the highest activity against APOBEC3G that was ascribed to its increased binding activity, for which the N-terminal domain of the Vif protein sequences was responsible. These results suggest that the biological differences of Vif proteins belonging to different subtypes might affect viral fitness and quasispecies in vivo.
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