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dc.contributor.authorEgawa, Nagayasuen
dc.contributor.authorEgawa, Kiyofumien
dc.contributor.authorGriffin, Heatheren
dc.contributor.authorDoorbar, Johnen
dc.date.accessioned2015-07-15T11:06:41Z
dc.date.available2015-07-15T11:06:41Z
dc.date.issued2015-07-16en
dc.identifier.citationEgawa et al. Viruses (2015) Vol. 7 Issue 7, pp. 3863-3890. doi: 10.3390/v7072802en
dc.identifier.issn1999-4915
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/248970
dc.description.abstractPapillomaviruses have evolved over many millions of years to propagate themselves at specific epithelial niches in a range of different host species. This has lead 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 Alpha HPV 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.
dc.description.sponsorshipThe Human Papillomavirus Research Group at the University of Cambridge is funded by the UK Medical Research Council.
dc.languageEnglishen
dc.language.isoenen
dc.publisherMDPI
dc.rightsAttribution 2.0 UK: England & Wales*
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/uk/*
dc.subjectHuman Papillomavirusen
dc.subjecttropismen
dc.subjectdiversityen
dc.subjectevolutionen
dc.subjecttissue stem cellsen
dc.subjectnicheen
dc.subjectcarcinogenesisen
dc.titleHuman Papillomaviruses; Epithelial Tropisms, and the Development of Neoplasiaen
dc.typeArticle
dc.description.versionThis is the final version of the article. It first appeared from MDPI via http://dx.doi.org/10.3390/v7072802en
prism.endingPage3890
prism.publicationDate2015en
prism.publicationNameVirusesen
prism.startingPage3863
prism.volume7en
dc.rioxxterms.funderMRC
dcterms.dateAccepted2015-07-07en
rioxxterms.versionofrecord10.3390/v7072802en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2015-07-16en
dc.contributor.orcidEgawa, Nagayasu [0000-0002-3270-0592]
dc.contributor.orcidGriffin, Heather [0000-0002-4601-3064]
dc.contributor.orcidDoorbar, John [0000-0002-4027-102X]
dc.identifier.eissn1999-4915
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idMRC (MC_PC_13050)


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Attribution 2.0 UK: England & Wales
Except where otherwise noted, this item's licence is described as Attribution 2.0 UK: England & Wales