ArticleRetrovirology2018
Natural APOBEC3C variants can elicit differential HIV-1 restriction activity.
Article in Retrovirology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- A scalable two-step genome editing strategy for generating full-length gene-humanized mice at diverse genomic loci.Nature communications · 2026Article
- APOBEC3C coordinates DDX5 in R-loop resolution and dynamic control of Chk1-mediated stress-responsive circuitry as a prerequisite for gemcitabine resistance in p53-deficient cells.Cell death & disease · 2026Article
- HIV-1 latency: From acquaintance to confidant.Journal of virus eradication · 2025Review
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- Article
- APOBEC3F Is a Mutational Driver of the Human Monkeypox Virus Identified in the 2022 Outbreak.The Journal of infectious diseases · 2023Article
- Article
- Clinical Implications of APOBEC3-Mediated Mutagenesis in Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Review
- 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
- APOBEC3C, a nucleolar protein induced by genotoxins, is excluded from DNA damage sites.The FEBS journal · 2022Article
- Divergence in Dimerization and Activity of Primate APOBEC3C.Journal of molecular biology · 2021Article
- APOBEC3F Constitutes a Barrier to Successful Cross-Species Transmission of Simian Immunodeficiency Virus SIVsmm to Humans.Journal of virology · 2021Article
- Human APOBEC3 Variations and Viral Infection.Viruses · 2021Review
- SARS-CoV-2 spike L452R variant evades cellular immunity and increases infectivity.Cell host & microbe · 2021Article
- Potential Utilization of APOBEC3-Mediated Mutagenesis for an HIV-1 Functional Cure.Frontiers in microbiology · 2021Review
- Retroviral Restriction Factors and Their Viral Targets: Restriction Strategies and Evolutionary Adaptations.Microorganisms · 2020Review
- Association between APOBEC3s and HPV16 E2 gene hypermutation in Uygur females with cervical cancer.Oncology letters · 2020Article
- Article
- Structural perspectives on HIV-1 Vif and APOBEC3 restriction factor interactions.Protein science : a publication of the Protein Society · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe APOBEC3 (A3) family of DNA cytosine deaminases provides an innate barrier to infection by retroviruses including HIV-1. A total of five enzymes, A3C, A3D, A3F, A3G and A3H, are degraded by the viral accessory protein Vif and expressed at high levels in CD4+ T cells, the primary reservoir for HIV-1 replication in vivo. Apart from A3C, all of these enzymes mediate restriction of Vif-deficient HIV-1. However, a rare variant of human A3C (Ile188) was shown recently to restrict Vif-deficient HIV-1 in a 293T-based single cycle infection system. The potential activity of this naturally occurring A3C variant has yet to be characterized in a T cell-based spreading infection system. Here we employ a combination of Cas9/gRNA disruption and transient and stable protein expression to assess the roles of major Ser188 and minor Ile188 A3C variants in HIV-1 restriction in T cell lines.
resultsCas9-mediated mutation of endogenous A3C in the non-permissive CEM2n T cell line did not alter HIV-1 replication kinetics, and complementation with A3C-Ser188 or A3C-Ile188 was similarly aphenotypic. Stable expression of A3C-Ser188 in the permissive T cell line SupT11 also had little effect. However, stable expression of A3C-Ile188 in SupT11 cells inhibited Vif-deficient virus replication and inflicted G-to-A mutations.
conclusionsA3C-Ile188 is capable of inhibiting Vif-deficient HIV-1 replication in T cells. Although A3C is eclipsed by the dominant anti-viral activities of other A3s in non-permissive T cell lines and primary T lymphocytes, this enzyme may still be able to contribute to HIV-1 diversification in vivo. Our results highlight the functional redundancy in the human A3 family with regards to HIV-1 restriction and the need to consider naturally occurring variants.
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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 Socratic graph.