ArticleProceedings of the National Academy of Sciences of the United States of America2016
A critical role for alternative polyadenylation factor CPSF6 in targeting HIV-1 integration to transcriptionally active chromatin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers.
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Who cites it
191 citing papers in PubMed, 261 citations in OpenAlex.
- Host soluble inositol phosphate signaling promotes coronavirus replication.bioRxiv : the preprint server for biology · 2026Article
- Mechanistic Insights into HIV-1 Capsid Interactions with CPSF6.bioRxiv : the preprint server for biology · 2026Article
- Core nucleosomes are refractory to lentiviral DNA integration.Nature communications · 2026Article
- Capsid and integrase play essential apposing roles in viral ribonucleoprotein assembly during HIV-1 core morphogenesis.iScience · 2026Article
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- HIV capsid inhibitors: Mechanisms, resistance, and therapeutic advances.PLoS pathogens · 2026Review
- Block-and-Lock Approaches for HIV Cure: Mechanistic Insights, Challenges, and Emerging Role of CPSF6.International journal of molecular sciences · 2026Review
- HIV-1 uncoating location dictates sites of integration.Nature communications · 2026Article
- Relationship between the distribution of LEDGF along genes and positions of HIV-1 DNA integration.mBio · 2026Article
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- HIV-1 Integration Site Determines the Transcriptional Fate and Persistence of Integrated Proviruses.bioRxiv : the preprint server for biology · 2026Article
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- Lenacapavir-induced capsid damage uncovers HIV-1 genomes emanating from nuclear speckles.The EMBO journal · 2026Article
- Alternative polyadenylation upon CPSF6 knock-out enhances HIV-1 infection in primary T cells.PLoS pathogens · 2025Article
- Oligomeric HIV-1 integrase structures reveal functional plasticity for intasome assembly and RNA binding.Nature communications · 2025Article
- Preclinical virology profiles of the HIV-1 capsid inhibitors VH4004280 and VH4011499.Antimicrobial agents and chemotherapy · 2025Article
- Lenacapavir-induced Lattice Hyperstabilization is Central to HIV-1 Capsid Failure at the Nuclear Pore Complex and in the Cytoplasm.bioRxiv : the preprint server for biology · 2025Article
- Elucidating the mechanism by which HIV-1 nucleocapsid mutations confer resistance to integrase strand transfer inhibitors.Science advances · 2025Article
131 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Integration is vital to retroviral replication and influences the establishment of the latent HIV reservoir. HIV-1 integration favors active genes, which is in part determined by the interaction between integrase and lens epithelium-derived growth factor (LEDGF)/p75. Because gene targeting remains significantly enriched, relative to random in LEDGF/p75 deficient cells, other host factors likely contribute to gene-tropic integration. Nucleoporins 153 and 358, which bind HIV-1 capsid, play comparatively minor roles in integration targeting, but the influence of another capsid binding protein, cleavage and polyadenylation specificity factor 6 (CPSF6), has not been reported. In this study we knocked down or knocked out CPSF6 in parallel or in tandem with LEDGF/p75. CPSF6 knockout changed viral infectivity kinetics, decreased proviral formation, and preferentially decreased integration into transcriptionally active genes, spliced genes, and regions of chromatin enriched in genes and activating histone modifications. LEDGF/p75 depletion by contrast preferentially altered positional integration targeting within gene bodies. Dual factor knockout reduced integration into genes to below the levels observed with either single knockout and revealed that CPSF6 played a more dominant role than LEDGF/p75 in directing integration to euchromatin. CPSF6 complementation rescued HIV-1 integration site distribution in CPSF6 knockout cells, but complementation with a capsid binding mutant of CPSF6 did not. We conclude that integration targeting proceeds via two distinct mechanisms: capsid-CPSF6 binding directs HIV-1 to actively transcribed euchromatin, where the integrase-LEDGF/p75 interaction drives integration into gene bodies.
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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 OpenQuestion graph.