Related Experiment Video
Updated: Jun 23, 2026

Generation of Organotypic Raft Cultures from Primary Human Keratinocytes
Published on: February 22, 2012
Papillomavirus and disease in humans and animals
1Institute of Comparative Medicine, Glasgow University Veterinary School, Glasgow, UK. s.campo@vet.gla.ac.uk
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.
Related Concept Videos
Viral Recombination
Mechanisms of Retrovirus-induced Cancers
Mechanisms of Retrovirus-induced Cancers
Poliomyelitis
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...

