IMR Press / FBL / Volume 13 / Issue 3 / DOI: 10.2741/2739

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Papillomavirus E6 and E7 proteins and their cellular targets
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1 Division of Hematology/Oncology, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center and The University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA

Academic Editor: Rashmi Hegde

Front. Biosci. (Landmark Ed) 2008, 13(3), 1003–1017; https://doi.org/10.2741/2739
Published: 1 January 2008
(This article belongs to the Special Issue Structure-function analyses of papillomavirus proteins)
Abstract

The mucosal human papillomaviruses (HPVs) infect human genital and oral epithelial cells and cause lesions ranging in severity from benign to malignant. HPV associated malignancies include cervical and other anogenital cancers as well as a subpopulation of head and neck cancers. Viral infection of epidermal stem or transit amplifying cells can result in long term viral persistence, and the development of carcinogenesis over a significant amount of time then requires additional cooperating genetic hits. Only the so-called high risk HPV types mediate human carcinogenesis, whereas the low risk HPVs have been linked to benign epithelial lesions that are not generally life threatening, but nonetheless are a major health burden. Expression of the high risk HPV E6 and E7 oncogenes is sufficient for primary human keratinocyte immortalization and is required for initiation and all subsequent stages of carcinogenic progression. Together with the finding that high levels of E6/E7 are a unifying hallmark of HPV positive cancers, these two genes are presumed to be the relevant virus-derived transformation stimuli in humans. E6 and E7 proteins do not possess intrinsic enzymatic activities, but instead function though a number of direct and indirect interactions with cellular proteins, a number of which are well known cellular tumor suppressors. We will summarize here current insights into E6 and E7 interactions with specific cellular targets that stimulate aspects of the viral life cycle, interfere with cell cycle controls and promote carcinogenic processes.

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