Evidence map›Paper›PMID 26289843›Full record

ArticleThe Journal of general virology2015

Interaction of human papillomavirus type 16 particles with heparan sulfate and syndecan-1 molecules in the keratinocyte extracellular matrix plays an active role in infection.

Zurab Surviladze, Rosa T Sterkand, Michelle A Ozbun

Open access · greenAbstract read
In one paragraph

Article in The Journal of general virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.1field-weighted citation impact, top 25% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. 3D Tissue Culture Model for Virology Studies.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  8. Article
  9. 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) · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. The Key Role of Lysosomal Protease Cathepsins in Viral Infections.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Zurab SurviladzeDepartment of Molecular Genetics & Microbiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA.
Rosa T SterkandDepartment of Molecular Genetics & Microbiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA.
Michelle A OzbunDepartment of Molecular Genetics & Microbiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA.
University of New Mexico · US

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
Entry of Oncogenic HPVs into Human KeratinocytesR01CA132136 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI OZBUN, MICHELLE A · 2009 to 2013
$1.6M
NCI NIH HHS CA132136NCI NIH HHS P30 CA118100NCI NIH HHS R01 CA132136
6 · The paper itself

Abstract

Oncogenic human papillomaviruses (HPVs) attach predominantly to extracellular matrix (ECM) components during infection of cultured keratinocytes and in the rodent vaginal challenge model in vivo. However, the mechanism of virion transfer from the ECM to receptors that mediate entry into host cells has not been determined. In this work we strove to assess the role of heparan sulfate (HS) chains in HPV16 binding to the ECM and determine how HPV16 release from the ECM is regulated. We also assessed the extent to which capsids released from the ECM are infectious. We show that a large fraction of HPV16 particles binds to the ECM via HS chains, and that syndecan-1 (snd-1) molecules present in the ECM are involved in virus binding. Inhibiting the normal processing of snd-1 and HS molecules via matrix metalloproteinases and heparanase dramatically reduces virus release from the ECM, cellular uptake and infection. Conversely, exogenous heparinase activates each of these processes. We confirm that HPV16 released from the ECM is infectious in keratinocytes. Use of a specific inhibitor shows furin is not involved in HPV16 release from ECM attachment factors and corroborates other studies showing only the intracellular activity of furin is responsible for modulating HPV infectivity. These data suggest that our recently proposed model, describing the action of HS proteoglycan processing enzymes in releasing HPV16 from the cell surface in complex with the attachment factor snd-1, is also relevant to the release of HPV16 particles from the ECM to promote efficient infection of keratinocytes.

Indexed as

Extracellular MatrixFemaleHeparan SulfateHuman papillomavirus 16HumansKeratinocytesPapillomavirus InfectionsReceptors, VirusSyndecan-1Virus AttachmentHeparan SulfateReceptors, VirusSyndecan-1

Identifiers

PMID26289843
PMCPMC4681067
OpenAlexW2001591247

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.