ABSTRACT
References Papillomaviruses (PVs) are small DNA viruses that infect numerous vertebrate hosts, including humans. Viral infection targets epithelial cells and progeny virions are produced upon cellular differentiation. Although infection with most of the 85 human viral types identified to date leads to benign hyperproliferative lesions or warts,1 typically on the extremities, a small number of human PVs (HPVs) are causally associated with the development of anogenital cancer. Such oncogenic HPVs include types 16, 18, 31, 33 and 35, and are referred to as high-risk viruses to indicate the high probability for malignant progression after infection.2 Other HPVs associated with human neoplasia are epidermodysplasia verruciformis (EV)inducing types. This rare form of skin cancer may result from infection with HPV types 5 or 8 if the host has a genetic predisposition for EV. All PVs infect keratinocytes, and are believed to initiate infection through microscopic lacerations in the epithelium, which provides access to basal cells. Only the fibropapillomaviruses of ungulate animals can infect dermal fibroblasts as well as epithelial host cells. HPVs exhibit a high degree of tissue tropism and specific viral types infect either the cutaneous epithelium or the oral/genital mucosa. All PVs are disseminated by direct contact and genital HPVs are usually transmitted sexually.3 HPV epidemiology is described in Chapter 3 and the clinical manifestations of viral infections in Chapter 4.
