ArticleScience advances2023
HPV is a cargo for the COPI sorting complex during virus entry.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Distinct roles of COPI proteins attenuated in cell senescence.Science advances · 2026Article
- ARFGAP1 serves as a critical host factor during E30 infection: QS11 inhibits viral pathogenesis in hFcRn-IFNARVirology journal · 2025Article
- The nuclear import receptor importin-7 targets HPV from the Golgi to the nucleus to promote infection.Science advances · 2025Article
- From Viral Infection to Genome Reshaping: The Triggering Role of HPV Integration in Cervical Cancer.International journal of molecular sciences · 2025Review
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- COP I vesicles facilitate classical swine fever virus proliferation by transporting fatty acid synthase from the Golgi apparatus to the endoplasmic reticulum.Journal of virology · 2025Article
- Papillomavirus-like particles as vectors forMolecular therapy. Nucleic acids · 2025Article
- Article
- The cytoplasmic tail of IBV spike mediates intracellular retention via interaction with COPI-coated vesicles in retrograde trafficking.Journal of virology · 2025Article
- Article
- The BICD2 dynein cargo adaptor binds to the HPV16 L2 capsid protein and promotes HPV infection.PLoS pathogens · 2024Article
- Sequence-independent activity of a predicted long disordered segment of the human papillomavirus type 16 L2 capsid protein during virus entry.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Noncanonical Rab9a action supports retromer-mediated endosomal exit of human papillomavirus during virus entry.PLoS pathogens · 2023Article
- Crystal Structures of Plk1 Polo-Box Domain Bound to the Human Papillomavirus Minor Capsid Protein L2-Derived Peptide.Journal of microbiology (Seoul, Korea) · 2023Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
During entry, human papillomavirus (HPV) traffics from the cell surface to the endosome and then to the trans-Golgi network (TGN) and Golgi apparatus. HPV must transit across the TGN/Golgi and exit these compartments to reach the nucleus to cause infection, although how these steps are accomplished is unclear. Combining cellular fractionation, unbiased proteomics, and gene knockdown strategies, we identified the coat protein complex I (COPI), a highly conserved protein complex that facilitates retrograde trafficking of cellular cargos, as a host factor required for HPV infection. Upon TGN/Golgi arrival, the cytoplasmic segment of HPV L2 binds directly to COPI. COPI depletion causes the accumulation of HPV in the TGN/Golgi, resembling the fate of a COPI binding-defective L2 mutant. We propose that the L2-COPI interaction drives HPV trafficking through the TGN and Golgi stacks during virus entry. This shows that an incoming virus is a cargo of the COPI complex.
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