Abstract
Papillomavirus (PV) induces exophytic lesions (papillomas, warts) and flat lesions (flat warts, cervical intraepithelial neoplasia) in cutaneous and mucosal epithelia. The lesions are usually benign and generally regress without eliciting any serious clinical problems in a host but occasionally persist. Persistent lesions can be debilitating and can also provide a focus for malignant transformation to squamous cell carcinoma, particularly in the presence of environmental or genetic cofactors. This has been experimentally demonstrated in animals, particularly in cattle, where bovine PV (BPV)-induced papillomas progress to cancer of the upper gastrointestinal (GI) tract and the urinary bladder in animals exposed to bracken fern in the pasture, and in rabbits, where the progression of skin papillomas to squamous cell carcinoma depends on a particular variant of cottontail rabbit PV (CRPV) and on the major histocompatibility complex (MHC) class II haplotype of the animal. In this review, various aspects of the biology of BPV and CRPV are described and compared with those of human PV, including viral genome structure, regulation of transcription of the viral oncogenes, function of the viral oncoproteins, co-operation between virus and cofactors, virus latency, immunity and vaccination.
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