Papillomaviruses in anogenital cancer as a model to understand the role of viruses in human cancers.

Abstract

Infections with specific types of human papillomaviruses (HPV) have emerged as necessary but not sufficient factors for the development, at least, of the majority of cervical, vulvar, penile, and perianal cancers. Evidence has accumulated for their causal role in the induction of anogenital premalignant lesions. Genetic events underlying the mechanism of anogenital carcinogenesis have become increasingly understood. A host cell-mediated intracellular control down-regulating specific HPV genes (E6, E7) in replicating normal cells appears to be interrupted in cancer cells, probably due to structural modifications of the respective host cell genes acquired in the course of HPV DNA persistence. Since genital HPV infections are ubiquitous, cofactors which modify controlling host cell genes are likely to determine the different geographic rates of cervical cancer incidence.