The human papillomavirus (HPV) is the cause of multiple neoplastic conditions including recurrent respiratory papillomatosis and invasive cervical carcinoma. Despite the extremely high incidence rate of infection with HPV, the virus is normally cleared from the body, and disease states are only seen in a small subset of exposed individuals. There are over 120 different HPV types, each with distinct characteristics. The HPV genome encodes for seven early-expressed proteins (E1-7) and two late-expressed proteins (L1-2). The viral life cycle is tightly linked with normal physiology of cutaneous and mucosal stratified squamous epithelial tissues. In HPV-infected cells, progression toward neoplasia requires that the virus evades immune detection and clearance. Viral factors are able to co-opt normal homeostatic processes within infected squamous epithelial tissues to establish persistent infections, evade host immune detection, and activate neoplastic pathways. Key oncoproteins E6 and E7 exert their function through multiple mechanisms to drive neoplastic processes in both benign and malignant lesions. This chapter provides an overview of the key molecular features of the HPV family of viruses and their pathogenic mechanisms.
CITATION STYLE
Lambie, M., & Bratman, S. V. (2017). Fundamental biology of human papillomaviruses. In Recurrent Respiratory Papillomatosis (pp. 1–17). Springer International Publishing. https://doi.org/10.1007/978-3-319-63823-2_1
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