ArticleCellular microbiology2013
Heparin increases the infectivity of Human Papillomavirus type 16 independent of cell surface proteoglycans and induces L1 epitope exposure.
Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 66 citations in OpenAlex.
- Atomic resolution structure of human papillomavirus bound to heparin.Nature communications · 2026Article
- Multivalency influences virus dynamics at the glycocalyx: A study of glycosaminoglycan binding in HPV16 entry.Biophysical journal · 2026Article
- Filamentous virions act as non-infectious interfering particles to modulate papillomavirus infection.Journal of virology · 2026Article
- The actin nucleation promoting factor WASH facilitates clathrin-independent endocytosis of human papillomaviruses.EMBO reports · 2025Article
- HSPG-binding peptide Pep19-2.5 is a potent inhibitor of HPV16 infection.Antimicrobial agents and chemotherapy · 2025Article
- Glycan-induced structural activation softens the human papillomavirus capsid for entry through reduction of intercapsomere flexibility.Nature communications · 2024Article
- Site-specific sulfations regulate the physicochemical properties of papillomavirus-heparan sulfate interactions for entry.Science advances · 2024Article
- Folliculin Prevents Lysosomal Degradation of Human Papillomavirus To Support Infectious Cell Entry.Journal of virology · 2023Article
- Effect of Glycosaminoglycans onApplied and environmental microbiology · 2023Article
- Master mitotic kinases regulate viral genome delivery during papillomavirus cell entry.Nature communications · 2023Article
- Chondroitin Sulfate Proteoglycans Are De Facto Cellular Receptors for Human Papillomavirus 16 under High Serum Conditions.Journal of virology · 2022Article
- HPV16 Entry into Epithelial Cells: Running a Gauntlet.Viruses · 2021Review
- The long and winding road: human papillomavirus entry and subcellular trafficking.Current opinion in virology · 2021Review
- A Ran-binding protein facilitates nuclear import of human papillomavirus type 16.PLoS pathogens · 2021Article
- Advances in Targeting HPV Infection as Potential Alternative Prophylactic Means.International journal of molecular sciences · 2021Review
- Vesicular trafficking permits evasion of cGAS/STING surveillance during initial human papillomavirus infection.PLoS pathogens · 2020Article
- p120 catenin recruits HPV to γ-secretase to promote virus infection.PLoS pathogens · 2020Article
- Epidermal Growth Factor Receptor and Abl2 Kinase Regulate Distinct Steps of Human Papillomavirus 16 Endocytosis.Journal of virology · 2020Article
- In Vitro Organotypic Systems to Model Tumor Microenvironment in Human Papillomavirus (HPV)-Related Cancers.Cancers · 2020Review
- Infectious Entry of Merkel Cell Polyomavirus.Journal of virology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Human Papillomaviruses (HPVs) are the etiological agents of cervical cancer, and HPV-16 is the most prevalent type. Several HPVs require heparan sulfate proteoglycans (HSPGs) for cell binding. Here, we analyse the phenomenon that preincubation of HPV-16 with increasing concentrations of heparin results in partial restoration rather than more efficient inhibition of infection. While corroborating that the HSPGs are cell-binding receptors for HPV-16, heparin-preincubated virus bound to the extracellular matrix (ECM) via laminin-332. Furthermore, the interaction of virions with heparin, a representative of the highly sulfated S-domains of heparan sulfate (HS) chains of HSPGs, allowed HPV-16 infection in the absence of cell surface HSPGs. Therefore, we concluded that specific glycan moieties but not specific HSPG protein backbones are required for infection. The increased binding of an epitope-specific antibody to the viral capsid after heparin binding suggested that initial conformational changes in the HPV-16 virion occur during infection by interaction with'heparin-like' domains of cellular HSPGs. We propose that HS sequences with specific sulfation patterns are required to facilitate HPV-16 infection.
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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.