ArticlePLoS pathogens2012
Essential roles for soluble virion-associated heparan sulfonated proteoglycans and growth factors in human papillomavirus infections.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
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Who cites it
123 citing papers in PubMed, 175 citations in OpenAlex.
- Inhibition of Langerhans cell maturation by human papillomavirus type 16: a novel role for the annexin A2 heterotetramer in immune suppression.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Rab14 regulates the transport of human papillomavirus to the trans-Golgi network for infectious cell entry.FEBS letters · 2026Article
- Article
- The Role of HPV and Hormone in Cervical Precancer and Cancer: Molecular Pathophysiology and Cell Biology of Disease and Treatment.Oncology research · 2026Review
- Association of ABO Blood Groups with HPV Genotypes and Cervical Lesions in HPV-Positive Women.International journal of women's health · 2026Article
- The actin nucleation promoting factor WASH facilitates clathrin-independent endocytosis of human papillomaviruses.EMBO reports · 2025Article
- Targeting ferroptosis for precision medicine in cervical cancer.Apoptosis : an international journal on programmed cell death · 2025Review
- Human papilloma virus (HPV) mediated cancers: an insightful update.Journal of translational medicine · 2025Review
- Human Papillomavirus Type 16 Stimulates WAVE1- and WAVE2-Dependent Actin Protrusions for Endocytic Entry.Viruses · 2025Article
- Sexually transmitted human papillomavirus and related sequelae.Clinical microbiology reviews · 2025Review
- HSPG-binding peptide Pep19-2.5 is a potent inhibitor of HPV16 infection.Antimicrobial agents and chemotherapy · 2025Article
- Immune responses to human papillomavirus infection and vaccination.Frontiers in immunology · 2025Review
- Glycan-induced structural activation softens the human papillomavirus capsid for entry through reduction of intercapsomere flexibility.Nature communications · 2024Article
- The effects of metabolites from three vaginal bacteria on the Syndecan-1 of cervical epithelial cells.Heliyon · 2024Article
- Genetic predictors for bacterial vaginosis in women living with and at risk for HIV infection.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024Article
- Therapeutic development targeting host heparan sulfate proteoglycan in SARS-CoV-2 infection.Frontiers in medicine · 2024Review
- Targeting Cervical Cancer Stem Cells by Phytochemicals.Current medicinal chemistry · 2024Review
- Small Molecule Inhibitors of Human Papillomavirus: A Review of Research from 1997 to 2021.Current medicinal chemistry · 2024Review
- ErbB2/HER2 receptor tyrosine kinase regulates human papillomavirus promoter activity.Frontiers in immunology · 2024Article
- Review
63 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A subset of human papillomavirus (HPV) infections is causally related to the development of human epithelial tumors and cancers. Like a number of pathogens, HPV entry into target cells is initiated by first binding to heparan sulfonated proteoglycan (HSPG) cell surface attachment factors. The virus must then move to distinct secondary receptors, which are responsible for particle internalization. Despite intensive investigation, the mechanism of HPV movement to and the nature of the secondary receptors have been unclear. We report that HPV16 particles are not liberated from bound HSPG attachment factors by dissociation, but rather are released by a process previously unreported for pathogen-host cell interactions. Virus particles reside in infectious soluble high molecular weight complexes with HSPG, including syndecan-1 and bioactive compounds, like growth factors. Matrix mellatoproteinase inhibitors that block HSPG and virus release from cells interfere with virus infection. Employing a co-culture assay, we demonstrate HPV associated with soluble HSPG-growth factor complexes can infect cells lacking HSPG. Interaction of HPV-HSPG-growth factor complexes with growth factor receptors leads to rapid activation of signaling pathways important for infection, whereas a variety of growth factor receptor inhibitors impede virus-induced signaling and infection. Depletion of syndecan-1 or epidermal growth factor and removal of serum factors reduce infection, while replenishment of growth factors restores infection. Our findings support an infection model whereby HPV usurps normal host mechanisms for presenting growth factors to cells via soluble HSPG complexes as a novel method for interacting with entry receptors independent of direct virus-cell receptor interactions.
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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.