The virion of the Papovaviridae family of viruses contains a double-stranded circular DNA as the genome, has an icosahedral capsid, and can induce tumors in animals. The name papovavirus is derived from papillomavirus, polyomavirus, and vacuolating virus (the old name of SV40). The particle and genome sizes of papillomaviruses are slightly greater than those of polyomaviruses, measuring 55 nm in diameter instead of 45 nm, and about 8000 base pairs in length instead of about 5000. On this basis, the papovaviruses are divided into two genera, Polyomavirus and Papillomavirus. BKV, JCV, SV40, LPV, murine polyomavirus, hamster polyomavirus, and many others are classified in the former genus.
Papillomaviruses were isolated as agents that can induce warts in many animals, including rabbits, goats, cattle, dogs, deer, and so on. Papillomaviruses were also isolated from human warts in late 1970s. Presently, more than 70 viruses are classified as human papillomavirus (HPV). A subgroup of about 20 HPVs has been associated with lesions of the anogenital tract. These HPVs can be further divided into two groups: the low-risk HPV group, including HPV 6 and HPV 11, which are associated with benign lesions, such as condyloma acuminata, and the high-risk group, including HPV16, HPV18, HPV33, and others, which are associated with malignant lesions that can progress to cancer. The high-risk HPV can efficiently immortalize human squamous epithelial cells in vitro and transform established rodent cells. The genes of the high-risk group HPVs that are responsible for the transforming activity are E6 and E7, which are ubiquitously conserved among all papilloma viruses, including those of animal origins. The E7 gene products of the high-risk HPVs bind and inactivate retinoblastoma family proteins more efficiently than those of the low-risk HPVs and HPVs associated with benign skin lesions. This binding is mediated through the amino acid sequence of the E7 gene product, which is commonly detected in the large T antigens of SV40 and polyomaviruses. The only E6 gene products of the high-risk groups bind to p53 protein through an interaction with cellular E6-AP protein, and they subsequently cause the ubiquitin-mediated protein degradation of the p53 protein. The consequent deregulation of cellular growth control by e6 and E7 genes is considered to be the molecular basis of carcinogenesis by the high-risk HPVs.
