Molecular evolution of papillomaviruses

Abstract
Introduction Papillomaviruses (PVs) are members of the genus Papillomavirus which, along with viruses of the genus Polyomavirus, comprise the family Papovaviridae (papillomavirus, polyomavirus and vacuolating agent). PVs are small, non-enveloped structures with icosahedral symmetry and a circular double-stranded DNA genome. They infect humans in addition to multiple other animal vertebrate species, resulting in a variety of proliferative epithelial lesions and tumours. Most papillomaviruses are species specific and have a cellular tropism for squamous epithelial cells. In benign papillomatous lesions, the viral genomes replicate as extrachromosomal episomes in the nuclei of basal and suprabasal epithelial cells. Complete vegetative replication with production of intact virions is found in the superficial and differentiated epithelial cells. In contrast, malignant lesions do not support vegetative viral replication, but instead often contain an integrated disrupted viral genome. Sixty years ago, Richard Shope (1933) linked the presence of the cottontail rabbit papillomavirus (CRPV) to cutaneous papillomatosis in rabbits, and Francis Peyton Rous described the conversion of papilloma to squamous cell carcinoma in rabbits, initiating the field of tumour virology (Rous & Beard, 1935). Much of the current interest in papillomavirus research can be attributed to the recent association of human papillomaviruses (HPVs) with cervical cancer, one of the leading causes of cancer-attributed death in women. Most of our knowledge of PVs has been obtained during the last decade through the use of recombinant DNA techniques. The small double-stranded DNA genomes of PVs have been readily amenable to cloning and sequencing. In the absence of a serological classification, HPVs have been categorized according to their genotype.

This publication has 0 references indexed in Scilit: