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Human Papillomaviruses; Epithelial Tropisms, and the Development of Neoplasia

1
Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK
2
The Francis Crick Institute Mill Hill Laboratory, the Ridgeway, Mill Hill, London NW7 1AA, UK
3
Department of Dermatology, The Jikei University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo 105-0003, Japan
4
Department of Microbiology, Kitasato University School of Allied Health and Sciences, 1-15-1 Kitasato, Sagamihara, Kanagawa 252-0373, Japan
*
Author to whom correspondence should be addressed.
Academic Editor: Joanna Parish
Viruses 2015, 7(7), 3863-3890; https://doi.org/10.3390/v7072802
Received: 11 May 2015 / Revised: 3 July 2015 / Accepted: 7 July 2015 / Published: 16 July 2015
(This article belongs to the Special Issue Tumour Viruses)
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. View Full-Text
Keywords: human papillomavirus; tropism; diversity; evolution; tissue stem cells; niche; carcinogenesis human papillomavirus; tropism; diversity; evolution; tissue stem cells; niche; carcinogenesis
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Egawa, N.; Egawa, K.; Griffin, H.; Doorbar, J. Human Papillomaviruses; Epithelial Tropisms, and the Development of Neoplasia. Viruses 2015, 7, 3863-3890.

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