Similarities of papillomavirus infections with tumor promoters.
Papillomaviruses represent a group of small DNA-containing agents which differ in genetic organization and biological properties profoundly from other groups of viruses. Infection of cells of the basal cell layer by these viruses results in enhanced proliferation (papillomas) by retaining in part the differentiation pattern of normal cells. Virus production occurs in differentiated non-dividing cells of the stratum spinosum, granulosum, and corneum. Up to now the viruses cannot be propagated in tissue cultures. Cells induced to proliferation by papillomaviruses maintain the viral DNA frequently as free episomes in high copy number. The heterogeneity of the papillomavirus group has been revealed during the past few years. Presently 25 distinct types of human papillomaviruses have been characterized. Several animal and human systems have been reported in which papillomaviruses appear to contribute to malignant conversion. In most of these instances, besides infection by a specific type of papillomavirus, additional interaction with chemical or physical carcinogens (initiators) appears to be required. Papillomaviruses thus seem to reveal properties ascribed to tumor promoters. Moreover, clinical observations demonstrated an inhibition of papillomavirus infections by stage II inhibitors of tumor promotion, specifically by retionic acid. We investigated the role of papillomavirus infections in specific types of human cancer. Five types of papillomavirus infections (HPV 6, 10, 11, 16, and 18) were characterized in the human genital tract. HPV types 6, 10, and 11 were preferentially found in benign lesions (condylomate acuminata, cervical dysplasias), whereas HPV 16 prevails in malignant and in pre-malignant proliferations (cervical, vulval, and penile cancer, Bowenoid papulosis, Bowen's disease, carcinomata in situ).(ABSTRACT TRUNCATED AT 250 WORDS)
D000818:Animals; D002471:Cell Transformation, Neoplastic; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D005833:Genital Neoplasms, Female / Q000209:etiology / Q000382:microbiology; D005834:Genital Neoplasms, Male / Q000209:etiology / Q000382:microbiology; D006801:Humans; D008297:Male; D009369:Neoplasms / Q000209:etiology*; D027383:Papillomaviridae / Q000472:pathogenicity; D014412:Tumor Virus Infections / Q000150:complications*
D004279:DNA, Viral