RESEARCH ARTICLE


The HPV E2-Host Protein-Protein Interactions: A Complex Hijacking of the Cellular Network



Mandy Muller1, 2, Caroline Demeret*, 1
1 Unité de Génétique, Papillomavirus et Cancer Humain (GPCH), Institut Pasteur, 25 rue du Docteur Roux, 75015 Paris, France
2 Univ. Paris Diderot, Sorbonne Paris cite, Cellule Pasteur, rue du Docteur Roux, 75015 Paris, France

Article Information


Identifiers and Pagination:

Year: 2012
Volume: 6
Issue: Suppl 2
First Page: 173
Last Page: 189
Publisher Id: TOVJ-6-173
DOI: 10.2174/1874357901206010173

Article History:

Received Date: 25/6/2012
Revision Received Date: 20/7/2012
Acceptance Date: 30/7/2012
Electronic publication date: 28/12/2012
Collection year: 2012

© Muller and Demeret; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the “Unité de Génétique, Papillomavirus et Cancer Humain, Institut Pasteur, 25 rue du Dr Roux, 75724 Paris, France; Tel: +33 (0) 145 688 526; E-mail: caroline.demeret@pasteur.fr


Abstract

Over 100 genotypes of human papillomaviruses (HPVs) have been identified as being responsible for unapparent infections or for lesions ranging from benign skin or genital warts to cancer. The pathogenesis of HPV results from complex relationships between viral and host factors, driven in particular by the interplay between the host proteome and the early viral proteins. The E2 protein regulates the transcription, the replication as well as the mitotic segregation of the viral genome through the recruitment of host cell factors to the HPV regulatory region. It is thereby a pivotal factor for the productive viral life cycle and for viral persistence, a major risk factor for cancer development. In addition, the E2 proteins have been shown to engage numerous interactions through which they play important roles in modulating the host cell. Such E2 activities are probably contributing to create cell conditions appropriate for the successive stages of the viral life cycle, and some of these activities have been demonstrated only for the oncogenic high-risk HPV. The recent mapping of E2-host protein-protein interactions with 12 genotypes representative of HPV diversity has shed some light on the large complexity of the host cell hijacking and on its diversity according to viral genotypes. This article reviews the functions of E2 as they emerge from the E2/host proteome interplay, taking into account the large-scale comparative interactomic study.

Keywords: HPV, E2, protein interactions, network, viral pathogenesis, productive life cycle, cervical cancer..