ArticleNature microbiology2020
Vpu modulates DNA repair to suppress innate sensing and hyper-integration of HIV-1.
Article in Nature microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Single-cell profiling reveals IFI44L as a central regulator of immune dysregulation in high HIV viral load.Medical microbiology and immunology · 2026Article
- Protocol to differentially quantify spatially resolved viral protein-cellular protein interactions via proximity ligation assays.STAR protocols · 2026Article
- DNA damage induced by HIV-1 Vpr triggers epigenetic remodeling and transcriptional programs to enhance virus transcription and latency reactivation.PLoS biology · 2026Article
- Nef stabilizes actin to prevent HIV-1 sensing by RIG-I-like receptors.Nature communications · 2025Article
- HIV-1 Vpu interacts with RBM10 to promote HIV-1 infection.mSystems · 2025Article
- Article
- HIV-1 Vpr orchestrates ciTRAN upregulation through TGF-β induction.PLoS pathogens · 2025Article
- TRIM23 mediates cGAS-induced autophagy in anti-HSV defense.Nature communications · 2025Article
- SIV-specific neutralizing antibody induction following selection of a PI3K drive-attenuatedeLife · 2025Article
- The emerging roles of ubiquitin-like modifications in regulating HIV replication and host defense.Frontiers in cellular and infection microbiology · 2025Review
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- Review
- Inhibition of ATM-directed antiviral responses by HIV-1 Vif.PLoS pathogens · 2023Article
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- Acetylation of the NS3 helicase by KAT5γ is essential for flavivirus replication.Cell host & microbe · 2023Article
- ABRAXAS1 orchestrates BRCA1 activities to counter genome destabilizing repair pathways-lessons from breast cancer patients.Cell death & disease · 2023Article
- Endogenous IFITMs boost SARS-coronavirus 1 and 2 replication whereas overexpression inhibits infection by relocalizing ACE2.iScience · 2023Article
- A CRISPR-Cas Cure for HIV/AIDS.International journal of molecular sciences · 2023Review
- Workshop on RanBP2/Nup358 and acute necrotizing encephalopathy.Nucleus (Austin, Tex.) · 2022Article
- Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
To avoid innate sensing and immune control, human immunodeficiency virus type 1 (HIV-1) has to prevent the accumulation of viral complementary DNA species. Here, we show that the late HIV-1 accessory protein Vpu hijacks DNA repair mechanisms to promote degradation of nuclear viral cDNA in cells that are already productively infected. Vpu achieves this by interacting with RanBP2-RanGAP1*SUMO1-Ubc9 SUMO E3-ligase complexes at the nuclear pore to reprogramme promyelocytic leukaemia protein nuclear bodies and reduce SUMOylation of Bloom syndrome protein, unleashing end degradation of viral cDNA. Concomitantly, Vpu inhibits RAD52-mediated homologous repair of viral cDNA, preventing the generation of dead-end circular forms of single copies of the long terminal repeat and permitting sustained nucleolytic attack. Our results identify Vpu as a key modulator of the DNA repair machinery. We show that Bloom syndrome protein eliminates nuclear HIV-1 cDNA and thereby suppresses immune sensing and proviral hyper-integration. Therapeutic targeting of DNA repair may facilitate the induction of antiviral immunity and suppress proviral integration replenishing latent HIV reservoirs.
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