Human papillomaviruses: targeting differentiating epithelial cells for malignant transformation.
Human papillomavirus (HPV) infections play a crucial role in the pathogenesis of cervical neoplasia. Insights into the mechanisms by which HPV infection can, in a small numbers of cases, result in malignancy, comes from the observation that three proteins encoded by high-risk genital HPVs, E6, E7 and to a lesser extent E5, target factors that control the cell cycle and proliferation. These interactions result in abrogation of cell cycle control, chromosomal alterations, telomerase activation, and eventual cell immortalization. In this review, we discuss the functions of E6, E7, and E5 proteins that are most relevant to the malignant progression of HPV-transformed cells.
Fehrmann
Frauke
F
Department of Microbiology-Immunology, The Feinberg School of Medicine, Northwestern University, 303 E Chicago Ave., Chicago, IL 60611, USA.
Laimins
Laimonis A
LA
D002454:Cell Differentiation; D002455:Cell Division; D002471:Cell Transformation, Neoplastic; D004847:Epithelial Cells / Q000821:virology*; D016679:Genome, Viral; D006801:Humans; D008957:Models, Genetic; D009856:Oncogene Proteins, Viral / Q000502:physiology; D027383:Papillomaviridae / Q000472:pathogenicity*
D009856:Oncogene Proteins, Viral