Human Papillomaviruses; Epithelial Tropisms, and the Development of Neoplasia
Identifieur interne : 000047 ( Main/Exploration ); précédent : 000046; suivant : 000048Human Papillomaviruses; Epithelial Tropisms, and the Development of Neoplasia
Auteurs : Nagayasu Egawa [Royaume-Uni] ; Kiyofumi Egawa [Japon] ; Heather Griffin [Royaume-Uni] ; John Doorbar [Royaume-Uni]Source :
- Viruses [ 1999-4915 ] ; 2015.
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.
Url:
DOI: 10.3390/v7072802
PubMed: 26193301
PubMed Central: 4517131
Affiliations:
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Epithelial Tropisms, and the Development of Neoplasia</title><author><name sortKey="Egawa, Nagayasu" sort="Egawa, Nagayasu" uniqKey="Egawa N" first="Nagayasu" last="Egawa">Nagayasu Egawa</name><affiliation><nlm:aff id="af1-viruses-07-02802">Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK; E-Mails:<email>ne259@cam.ac.uk</email> (N.E.);<email>hmg36@cam.ac.uk</email> (H.G.)</nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-viruses-07-02802">The Francis Crick Institute Mill Hill Laboratory, the Ridgeway, Mill Hill, London NW7 1AA, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>The Francis Crick Institute Mill Hill Laboratory, the Ridgeway, Mill Hill, London NW7 1AA</wicri:regionArea><wicri:noRegion>London NW7 1AA</wicri:noRegion></affiliation></author><author><name sortKey="Egawa, Kiyofumi" sort="Egawa, Kiyofumi" uniqKey="Egawa K" first="Kiyofumi" last="Egawa">Kiyofumi Egawa</name><affiliation><nlm:aff id="af3-viruses-07-02802">Department of Dermatology, The Jikei University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo 105-0003, Japan; E-Mail:<email>amamino.kuroibo@gmail.com</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-viruses-07-02802">Department of Microbiology, Kitasato University School of Allied Health and Sciences, 1-15-1 Kitasato, Sagamihara, Kanagawa 252-0373, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Microbiology, Kitasato University School of Allied Health and Sciences, 1-15-1 Kitasato, Sagamihara, Kanagawa 252-0373</wicri:regionArea><wicri:noRegion>Kanagawa 252-0373</wicri:noRegion></affiliation></author><author><name sortKey="Griffin, Heather" sort="Griffin, Heather" uniqKey="Griffin H" first="Heather" last="Griffin">Heather Griffin</name><affiliation><nlm:aff id="af1-viruses-07-02802">Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK; E-Mails:<email>ne259@cam.ac.uk</email> (N.E.);<email>hmg36@cam.ac.uk</email> (H.G.)</nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-viruses-07-02802">The Francis Crick Institute Mill Hill Laboratory, the Ridgeway, Mill Hill, London NW7 1AA, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>The Francis Crick Institute Mill Hill Laboratory, the Ridgeway, Mill Hill, London NW7 1AA</wicri:regionArea><wicri:noRegion>London NW7 1AA</wicri:noRegion></affiliation></author><author><name sortKey="Doorbar, John" sort="Doorbar, John" uniqKey="Doorbar J" first="John" last="Doorbar">John Doorbar</name><affiliation><nlm:aff id="af1-viruses-07-02802">Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK; E-Mails:<email>ne259@cam.ac.uk</email> (N.E.);<email>hmg36@cam.ac.uk</email> (H.G.)</nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-viruses-07-02802">The Francis Crick Institute Mill Hill Laboratory, the Ridgeway, Mill Hill, London NW7 1AA, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>The Francis Crick Institute Mill Hill Laboratory, the Ridgeway, Mill Hill, London NW7 1AA</wicri:regionArea><wicri:noRegion>London NW7 1AA</wicri:noRegion></affiliation></author></analytic><series><title level="j">Viruses</title><idno type="eISSN">1999-4915</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>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.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Doorbar, J" uniqKey="Doorbar J">J. 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Kittler</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Japon</li><li>Royaume-Uni</li></country></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Egawa, Nagayasu" sort="Egawa, Nagayasu" uniqKey="Egawa N" first="Nagayasu" last="Egawa">Nagayasu Egawa</name></noRegion><name sortKey="Doorbar, John" sort="Doorbar, John" uniqKey="Doorbar J" first="John" last="Doorbar">John Doorbar</name><name sortKey="Griffin, Heather" sort="Griffin, Heather" uniqKey="Griffin H" first="Heather" last="Griffin">Heather Griffin</name></country><country name="Japon"><noRegion><name sortKey="Egawa, Kiyofumi" sort="Egawa, Kiyofumi" uniqKey="Egawa K" first="Kiyofumi" last="Egawa">Kiyofumi Egawa</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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