THE MALIGNANT POTENTIAL OF PAPILLOMAVIRUS *

SUMMARY Papillomaviruses are double‐stranded DNA viruses which can be classified into groups, types and subtypes on the basis of DNA cross‐hybridisation and restriction endonuclease patterns. In the majority of cases they produce a benign epithelial proliferation. However, restricted types can be associated with malignant transformation. Persistent papillomas in rabbits and oesophageal papillomas in immunosuppressed cattle develop into carcinomas. Human papillomavirus (HPV) is associated with cervical and laryngeal carcinomas. Immunosuppressed patients and those suffering from the rare autosomal recessive disease epidermodysplasia verruciformis have an increased incidence of papillomas andsquamous cell carcinomas (SCC) on sun‐exposed areas. The DNA of HPV types 5, 8 and 14 can be found in these SCC and in their rare metastases. Generally the SCC can be related to a previous wart and occur on sun‐exposed areas. The mechanism of tumour induction is not clear. There is no evidence for cell transformation by integration of a viral promoter in front of a cellular oncogene. The viral DNA remains extrachromosomal without major deletions or insertions. Viral papillomas undergoing malignant transformation on the skin require the addition of ultraviolet light for successful transformation. UVB is known to disrupt DNA, impair Langerhans cell number and function and, in mice, induce a subset of suppressor T cells which enhance the occurrence of cutaneous malignancy. This suggests a viral mutation and/or local immunosuppression in the transformation mechanism. Research on papillomavirus is greatly hindered by the inability to culture virions. This is probably related to difficulty producing fully differentiated keratinocytes in culture as well as the prolonged incubation period of the virus.