ArticleScientific reports2016
Translational regulation of APOBEC3G mRNA by Vif requires its 5'UTR and contributes to restoring HIV-1 infectivity.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Mechanisms of APOBEC3 Packaging into HIV-1.Viruses · 2026Review
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- Review
- The Disassociation of A3G-Related HIV-1 cDNA G-to-A Hypermutation to Viral Infectivity.Viruses · 2024Article
- HIV Infection: Shaping the Complex, Dynamic, and Interconnected Network of the Cytoskeleton.International journal of molecular sciences · 2023Review
- Host cell restriction factors of equine infectious anemia virus.Virologica Sinica · 2023Review
- A Conserved uORF Regulates APOBEC3G Translation and Is Targeted by HIV-1 Vif Protein to Repress the Antiviral Factor.Biomedicines · 2021Article
- Review
- Foamy Viruses, Bet, and APOBEC3 Restriction.Viruses · 2021Review
- The Role of APOBECs in Viral Replication.Microorganisms · 2020Review
- Induction of APOBEC3B cytidine deaminase in HTLV-1-infected humanized mice.Experimental and therapeutic medicine · 2019Article
- A quick guide for using Microsoft OneNote as an electronic laboratory notebook.PLoS computational biology · 2019Article
- Structural Determinants of the APOBEC3G N-Terminal Domain for HIV-1 RNA Association.Frontiers in cellular and infection microbiology · 2019Article
- A New Class of Antiretroviral Enabling Innate Immunity by Protecting APOBEC3 from HIV Vif-Dependent Degradation.Trends in molecular medicine · 2018Review
- APOBEC3G Regulation of the Evolutionary Race Between Adaptive Immunity and Viral Immune Escape Is Deeply Imprinted in the HIV Genome.Frontiers in immunology · 2018Article
- Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The essential HIV-1 viral infectivity factor (Vif) allows productive infection of non-permissive cells expressing cytidine deaminases APOBEC3G (A3G) and A3F by decreasing their cellular level, and preventing their incorporation into virions. Unlike the Vif-induced degradation of A3G, the functional role of the inhibition of A3G translation by Vif remained unclear. Here, we show that two stem-loop structures within the 5'-untranslated region of A3G mRNA are crucial for translation inhibition by Vif in cells, and most Vif alleles neutralize A3G translation efficiently. Interestingly, K26R mutation in Vif abolishes degradation of A3G by the proteasome but has no effect at the translational level, indicating these two pathways are independent. These two mechanisms, proteasomal degradation and translational inhibition, similarly contribute to decrease the cellular level of A3G by Vif and to prevent its incorporation into virions. Importantly, inhibition of A3G translation is sufficient to partially restore viral infectivity in the absence of proteosomal degradation. These findings demonstrate that HIV-1 has evolved redundant mechanisms to specifically inhibit the potent antiviral activity of A3G.
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