Abstract
There is mounting evidence that certain types of human papillomaviruses (HPV types 16 and 18) are associated with human genital cancer. Other virus types, such as HPV-6 or HPV-11, are more regularly found in benign genital warts. Since all viruses can be present in putative precancerous lesions of the uterine cervix (dysplasia, cervical intraepithelial neoplasia) it has been postulated that individual HPV types have different 'oncogenic potential'. The molecular basis for this difference is not known. The question of the natural reservoir for the oncogenic viruses is discussed. Expression of parts of the early region of the HPV genome in cell lines established from genital cancer supports the hypothesis that papillomaviruses are involved in inducing and/or maintaining the transformed phenotype of cancer cells.