ArticleJournal of virology2025
HIV-1 Nef activates proviral DNA transcription by recruiting Src kinase to phosphorylate host protein Nef-associated factor 1 to compromise its viral restrictive function.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Hijacking the Host: Post-Translational Modifications as Molecular Switches in HIV Persistence and Immune Evasion.Journal of medical virology · 2026Review
- Role of Src family kinases Fyn and Lyn in arenavirus infection.Journal of virology · 2026Article
- Molecular Investigation of Product Nkabinde in HIV Therapy: A Network Pharmacology and Molecular Docking Approach.International journal of molecular sciences · 2026Article
- Rewriting the viral script: post-translational modifications orchestrating SARS-CoV-2 pathogenesis and immune evasion.Frontiers in microbiology · 2026Review
- Beyond Viral Assembly: The Emerging Role of HIV-1 p17 in Vascular Inflammation and Endothelial Dysfunction.International journal of molecular sciences · 2025Review
- Cannabinoid Receptor Type 2 Agonist JWH-133 Stimulates Antiviral Factors and Decreases Proviral, Inflammatory, and Neurotoxic Proteins in HIV-Infected Macrophage Secretome.International journal of molecular sciences · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
HIV-1 accessory protein Nef is a multifunctional pathogenic factor that mediates immune evasion, enhances virion infectivity, antagonizes host restrictive factors, and promotes viral dissemination. However, the modulation of Nef on proviral DNA transcription of latently infected viruses is not well understood. In this study, we found that Nef activated HIV-1 proviral DNA transcription by recruiting Src Family Kinases (SFKs) member Src to stimulate the downstream PI3K/AKT/mTOCR1/CDK9 cellular pathway, and that Naf1 (Nef-associated factor 1), a host protein that is known to suppress HIV-1 transcription, was required for this function of Nef. This seemingly contradictory interplay between Nef and Naf1 was investigated. Naf1 was a repressor of the PI3K/AKT/mTOCR1/CDK9 cellular pathway, but in the presence of Nef, Naf1 was phosphorylated at the Tyrosine-552 by Nef-recruited Src, consequently converting its normal restrictive role to coordinate with Nef to activate proviral DNA transcription. These findings reveal a mechanism by which Nef activates HIV-1 proviral DNA transcription and discover the dual function of Naf1 protein in regulating HIV infection, depending on its phosphorylation status. This study reports a new interaction mode between host factors and viral proteins in regulating HIV-1 replication. IMPORTANCE: HIV-1 accessory protein Nef is a multifunctional pathogenic factor; however, the modulation of Nef on proviral DNA transcription of latently infected virus is not well understood. This study demonstrates Nef's role in activating HIV-1 proviral DNA transcription and uncovers the underlying cellular mechanism. Nef recruits Src kinase to phosphorylate Naf1, and the phosphorylation of Naf1 converts its normal restrictive role to coordinate with Nef to activate proviral DNA transcription by stimulating the downstream PI3K/AKT/mTOCR1/CDK9 cellular pathway. These findings also report a new interaction mode between host factors and viral proteins in regulating HIV-1 replication.
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