ReviewPapillomavirus research (Amsterdam, Netherlands)2019
Extracellular events impacting human papillomavirus infections: Epithelial wounding to cell signaling involved in virus entry.
Review in Papillomavirus research (Amsterdam, Netherlands), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- TGF-β-induced epithelial to mesenchymal transition drives proteoglycan binding specificity of HPV-based drug conjugates for cancer cells.Frontiers in oncology · 2026Article
- Immune responses to human papillomavirus infection and vaccination.Frontiers in immunology · 2025Review
- Cell-Free Expression of HPV16 Minor Capsid Protein L2 and Its Interaction with S100A10.Protein and peptide letters · 2025Article
- Article
- Biological, demographic, and health factors associated with HPV infection in Ecuadorian women.Frontiers in public health · 2023Article
- Human papillomavirus-related neoplasia of the ocular adnexa.Acta ophthalmologica · 2022Article
- HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation.International journal of molecular sciences · 2022Review
- Chondroitin Sulfate Proteoglycans Are De Facto Cellular Receptors for Human Papillomavirus 16 under High Serum Conditions.Journal of virology · 2022Article
- Protamine Sulfate Is a Potent Inhibitor of Human Papillomavirus InfectionAntimicrobial agents and chemotherapy · 2022Article
- CMV Seropositive Status Increases Heparanase SNPs Regulatory Activity, Risk of Acute GVHD and Yield of CD34Cells · 2021Article
- Exogenous Vimentin Supplementation Transiently Affects Early Steps during HPV16 Pseudovirus Infection.Viruses · 2021Article
- The long and winding road: human papillomavirus entry and subcellular trafficking.Current opinion in virology · 2021Review
- Causes and Consequences of HPV Integration in Head and Neck Squamous Cell Carcinomas: State of the Art.Cancers · 2021Review
- Heparan Sulfate Proteoglycans in Viral Infection and Treatment: A Special Focus on SARS-CoV-2.International journal of molecular sciences · 2021Review
- Advances in Targeting HPV Infection as Potential Alternative Prophylactic Means.International journal of molecular sciences · 2021Review
- Tetraspanin CD9 affects HPV16 infection by modulating ADAM17 activity and the ERK signalling pathway.Medical microbiology and immunology · 2020Article
- Theta-Defensins Inhibit High-Risk Human Papillomavirus Infection Through Charge-Driven Capsid Clustering.Frontiers in immunology · 2020Article
- Progress in eliminating HPV-associated disease.Papillomavirus research (Amsterdam, Netherlands) · 2019Article
- ADAM17-dependent signaling is required for oncogenic human papillomavirus entry platform assembly.eLife · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Human papillomaviruses (HPVs), like all PVs, predominantly cause benign tumors, or warts, in stratifying squamous epithelial tissues. Virions are released from apical surfaces of the skin and mucosa and, to initiate a new infection, must utilize a break in the epithelial barrier to access mitotically active basal epithelial cells. Laboratory models currently used to study the HPV infectious process reveal that heparan sulfate proteoglycans and cellular enzymes are utilized to prime virions and activate cell signaling to coordinate virus association with a receptor complex for uptake into keratinocytes. Conventional cell-based infection systems lack many aspects relevant to determining the role of epithelial wounding in HPV infections. Nevertheless, many cellular factors involved in virion interaction with cells have been shown to actively coordinate their activities in the dynamic state of an epithelial wound. In this review, I summarize the current knowledge regarding how HPVs interact with extracellular components to prime virus particles for eventual disassembly and effectuate association with the viral receptor complex. Additionally, I propose a model to account for how epithelial injury and the wound response may actively participate in successful HPV infection of basal epithelial cells.
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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.