Evidence map›Paper›PMID 26193301›Full record

ReviewViruses2015

Human Papillomaviruses; Epithelial Tropisms, and the Development of Neoplasia.

Nagayasu Egawa, Kiyofumi Egawa, Heather Griffin, John Doorbar

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 287 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
287citing papers in PubMed, 2 pooled it
27.0field-weighted citation impact, top 1% 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

287 citing papers in PubMed, 2 syntheses or guidelines pooled it, 556 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. HPV in oropharyngeal squamous papillomas: a missing link in head and neck viral pathogenesis.Virchows Archiv : an international journal of pathology · 2026
    Article
  10. Review
  11. Article
  12. Evidence for Anal Dysplasia Treatment.Clinics in colon and rectal surgery · 2026
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

227 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Nagayasu EgawaDivision of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK. ne259@cam.ac.uk.
Kiyofumi EgawaDepartment of Dermatology, The Jikei University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo 105-0003, Japan. amamino.kuroibo@gmail.com.
Heather GriffinDivision of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK. hmg36@cam.ac.uk.
John DoorbarDivision of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK. jd121@cam.ac.uk.
University of Cambridge · GBJikei University School of Medicine · JPThe Francis Crick Institute · GB

Funding

Medical Research Council MC_PC_13050
6 · The paper itself

Abstract

Papillomaviruses have evolved over many millions of years to propagate themselves at specific epithelial niches in a range of different host species. This has led to the great diversity of papillomaviruses that now exist, and to the appearance of distinct strategies for epithelial persistence. Many papillomaviruses minimise the risk of immune clearance by causing chronic asymptomatic infections, accompanied by long-term virion-production with only limited viral gene expression. Such lesions are typical of those caused by Beta HPV types in the general population, with viral activity being suppressed by host immunity. A second strategy requires the evolution of sophisticated immune evasion mechanisms, and allows some HPV types to cause prominent and persistent papillomas, even in immune competent individuals. Some Alphapapillomavirus types have evolved this strategy, including those that cause genital warts in young adults or common warts in children. These strategies reflect broad differences in virus protein function as well as differences in patterns of viral gene expression, with genotype-specific associations underlying the recent introduction of DNA testing, and also the introduction of vaccines to protect against cervical cancer. Interestingly, it appears that cellular environment and the site of infection affect viral pathogenicity by modulating viral gene expression. With the high-risk HPV gene products, changes in E6 and E7 expression are thought to account for the development of neoplasias at the endocervix, the anal and cervical transformation zones, and the tonsilar crypts and other oropharyngeal sites. A detailed analysis of site-specific patterns of gene expression and gene function is now prompted.

Indexed as

Viral TropismAnimalsEpithelial CellsGene Expression Regulation, ViralHumansNeoplasmsPapillomaviridaePapillomavirus InfectionsViral ProteinsViral Proteinscarcinogenesisdiversityevolutionhuman papillomavirusnichetissue stem cellstropism

Identifiers

PMID26193301
PMCPMC4517131
OpenAlexW1579431979

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.