ArticleeLife2019
HIV-1 nuclear import in macrophages is regulated by CPSF6-capsid interactions at the nuclear pore complex.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.
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Who cites it
148 citing papers in PubMed, 211 citations in OpenAlex.
- Mechanistic Insights into HIV-1 Capsid Interactions with CPSF6.bioRxiv : the preprint server for biology · 2026Article
- Hiding in Plain Sight: HIV-1 Membraneless Organelles as Nuclear Hubs-Host Hijacking, Replication, Immune Evasion, and Drug-Access Implications.Pathogens (Basel, Switzerland) · 2026Review
- HIV-1 capsid interactions with Nuclear Pore Complex components support nuclear entry via affinity gradient.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- HIV-1 uncoating location dictates sites of integration.Nature communications · 2026Article
- Stoichiometric binding of Cyclophilin-A to the HIV-1 capsid modulates its mechanoelastic properties.bioRxiv : the preprint server for biology · 2026Article
- Article
- Article
- Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication.FEMS microbiology reviews · 2026Review
- Lenacapavir-induced capsid damage uncovers HIV-1 genomes emanating from nuclear speckles.The EMBO journal · 2026Article
- Design, synthesis and profiling of highly potent antivirals targeting emerging drug-resistant HIV-1 variants.bioRxiv : the preprint server for biology · 2025Article
- Alternative polyadenylation upon CPSF6 knock-out enhances HIV-1 infection in primary T cells.PLoS pathogens · 2025Article
- Nuclear pore passage of the HIV capsid is driven by its unusual surface amino acid composition.Nature structural & molecular biology · 2025Article
- Direct visualization of HIV-1 core nuclear import and its interplay with the nuclear pore.EMBO reports · 2025Article
- Translocation of HIV capsid core through the Nuclear Pore Complex by affinity gradient.bioRxiv : the preprint server for biology · 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
- HIV-1 nuclear import is selective and depends on both capsid elasticity and nuclear pore adaptability.Nature microbiology · 2025Article
- IGF2BP2 binding to CPSF6 facilitates m6A-mediated alternative polyadenylation of PUM2 and promotes malignant progression in ovarian cancer.Clinical and translational medicine · 2025Article
- Retrointegration2023-Papers from the 7th International Conference on Retroviral Integration.Viruses · 2025Article
- Reverse transcription progression and genome length regulate HIV-1 core elasticity and disassembly.PLoS pathogens · 2025Article
88 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear entry of HIV-1 replication complexes through intact nuclear pore complexes is critical for successful infection. The host protein cleavage-and-polyadenylation-specificity-factor-6 (CPSF6) has been implicated in different stages of early HIV-1 replication. Applying quantitative microscopy of HIV-1 reverse-transcription and pre-integration-complexes (RTC/PIC), we show that CPSF6 is strongly recruited to nuclear replication complexes but absent from cytoplasmic RTC/PIC in primary human macrophages. Depletion of CPSF6 or lack of CPSF6 binding led to accumulation of HIV-1 subviral complexes at the nuclear envelope of macrophages and reduced infectivity. Two-color stimulated-emission-depletion microscopy indicated that under these circumstances HIV-1 complexes are retained inside the nuclear pore and undergo CA-multimer dependent CPSF6 clustering adjacent to the nuclear basket. We propose that nuclear entry of HIV-1 subviral complexes in macrophages is mediated by consecutive binding of Nup153 and CPSF6 to the hexameric CA lattice.
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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.