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Cross-talk of cutaneous beta human papillomaviruses and the immune system: determinants of disease penetrance.
Venuti, Assunta; Lohse, Stefan; Tommasino, Massimo; Smola, Sigrun.
Affiliation
  • Venuti A; 1 Infections and Cancer Biology Group, International Agency for Research on Cancer , 150 Cours Albert Thomas, Lyon 69008 , France.
  • Lohse S; 2 Institute of Virology, Saarland University Medical Center , Kirrbergerstr. Building 47, 66421 Homburg/Saar , Germany.
  • Tommasino M; 1 Infections and Cancer Biology Group, International Agency for Research on Cancer , 150 Cours Albert Thomas, Lyon 69008 , France.
  • Smola S; 2 Institute of Virology, Saarland University Medical Center , Kirrbergerstr. Building 47, 66421 Homburg/Saar , Germany.
Philos Trans R Soc Lond B Biol Sci ; 374(1773): 20180287, 2019 05 27.
Article in En | MEDLINE | ID: mdl-30955489
ABSTRACT
Human papillomaviruses (HPVs) infect the epithelia of skin or mucosa, where they can induce hyperproliferative lesions. More than 220 different HPV types have been characterized and classified into five different genera. Mucosal high-risk HPVs are causative for cancers of the anogenital region and oropharynx. Clinical data from patients with the rare genetic disorder epidermodysplasia verruciformis (EV) indicate that genus beta-HPVs cooperate with ultraviolet (UV) radiation in the development of cutaneous squamous cell carcinoma. In addition, epidemiological and biological findings indicate that beta-HPV types play a role in UV-mediated skin carcinogenesis also in non-EV individuals. However, the mechanisms used by these cutaneous viruses to promote epithelial carcinogenesis differ significantly from those of mucosal HPVs. Recent studies point to a delicate cross-talk of beta-HPVs with the cell-autonomous immunity of the host keratinocytes and the local immune microenvironment that eventually determines the fate of cutaneous HPV infection and the penetrance of disease. This review gives an overview of the critical interactions of genus beta-HPVs with the local immune system that allow the virus to complete its life cycle, to escape from extrinsic immunity, and eventually to cause chronic inflammation contributing to skin carcinogenesis. This article is part of the theme issue 'Silent cancer agents multi-disciplinary modelling of human DNA oncoviruses'.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Skin Neoplasms / Papillomavirus Infections / Disease Susceptibility / Betapapillomavirus / Immune System Type of study: Prognostic_studies Limits: Animals / Humans Language: En Journal: Philos Trans R Soc Lond B Biol Sci Year: 2019 Type: Article Affiliation country: France

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Skin Neoplasms / Papillomavirus Infections / Disease Susceptibility / Betapapillomavirus / Immune System Type of study: Prognostic_studies Limits: Animals / Humans Language: En Journal: Philos Trans R Soc Lond B Biol Sci Year: 2019 Type: Article Affiliation country: France