ArticleThe Journal of general virology2017
The cellular endosomal protein stannin inhibits intracellular trafficking of human papillomavirus during virus entry.
Article in The Journal of general virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Experimental Analysis of HPV16 L1/L2 Chimeric VLP Internalization by Human Peripheral Blood Leukocytes.International journal of molecular sciences · 2026Article
- The Rab5 effector Rabankyrin-5 mediates endosomal fusion and trafficking of human papillomavirus during early entry.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A Structural and Bioinformatics Investigation of a Fungal Squalene Synthase and Comparisons with Other Membrane Proteins.ACS omega · 2022Article
- The emerging roles of retromer and sorting nexins in the life cycle of viruses.Virologica Sinica · 2022Review
- Lessons in self-defence: inhibition of virus entry by intrinsic immunity.Nature reviews. Immunology · 2022Review
- Traptamer screening: a new functional genomics approach to study virus entry and other cellular processes.The FEBS journal · 2022Review
- HPV16 Entry into Epithelial Cells: Running a Gauntlet.Viruses · 2021Review
- Recent Advances in Our Understanding of the Infectious Entry Pathway of Human Papillomavirus Type 16.Microorganisms · 2021Review
- Advances in Targeting HPV Infection as Potential Alternative Prophylactic Means.International journal of molecular sciences · 2021Review
- From APOBEC to ZAP: Diverse mechanisms used by cellular restriction factors to inhibit virus infections.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Papillomaviruses and Endocytic Trafficking.International journal of molecular sciences · 2018Review
- Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Human papillomaviruses (HPVs) are the most common sexually transmitted viruses and one of the most important infectious causes of cancers worldwide. While prophylactic vaccines are effective against certain strains of HPV, established infections still cause deadly cancers in both men and women. HPV traffics to the nucleus via the retrograde transport pathway, but the mechanism of intracellular transport of non-enveloped viruses such as HPV is incompletely understood. Using an overexpression screen, we identify several genes that control HPV16 entry. We focused on the mechanism by which one of the screen hits, stannin, blocks HPV16 infection. Stannin has not been previously implicated in virus entry. Overexpression of stannin specifically inhibits infection by several HPV types, but not other viruses tested. Stannin is constitutively expressed in human keratinocytes, and its basal levels limit entry by HPV16. Stannin is localized to the endolysosomal compartment and does not affect HPV16 binding to cells, virus uptake, or virus uncoating, but inhibits the entry of HPV into the trans-Golgi network (TGN) and stimulates HPV degradation. We further show that stannin interacts with L1 major capsid protein and impairs the interaction of the L2 minor capsid protein with retromer, which is required for virus trafficking to the TGN. Our findings shed light on a novel cellular protein that interferes with HPV entry and highlight the role of retrograde transport in HPV entry.
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Registered trials
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.