Viral oncogenesis.

Human papillomaviruses (HPVs) are epitheliotropic viruses which cause a variety of lesions at cutaneous and mucosal sites. Lesions range from the benign wart to dysplasia and neoplasia. Importantly, HPV has been shown to be etiological in several malignancies including cervical cancer, other anogenital cancers, oropharyngeal cancers, and cutaneous malignancies in susceptible individuals, causing an estimated 5.2% of virally associated cancers worldwide. HPVs are small, double-stranded DNA viruses of the Papillomaviridae family; to date 150 genotypes have been characterized with approximately one third targeting mucosal sites. Studies of viral oncogenesis have revealed that HPV early genes interact with and modulate mediators of cell growth and cell cycle progression in the host cell. Recent studies have shed light on more novel mechanisms employed by viral oncoproteins including epigenetic modifications, modulating apoptosis pathways, affecting cell morphology and regulating angiogenesis. These recent studies demonstrate that our current understanding is still very limited and will continue to evolve with future research. The purpose of this chapter is to provide a general overview of HPV oncogenesis and to highlight several etiological questions that we hope will be answered by future research.