[Human papillomavirus and oncogenesis (author's transl)].
Various types of human papillomavirus (HPV) are responsible for different warts. Characteristic of HPV infections is a lowered cell-mediated immunity (CMI), especially defective in cases of epidermodysplasia verruciformis induced by HPV5. The malignant transformation seems to be related with the type of HPV, and not with the grade of CMI defect and duration of the infection. A life-long infection with HPV3 in cases of EV does not induce a malignant transformation in spite of heavily depressed CMI. The oncogenic potential has seemingly HPV5 responsible for red plaques and pityriasis versicolor-like lesions characteristic of EV. Malignant transformation, although rare, may also occur in long-lasting cases of genital warts (Buschke-Loewenstein-disease) and juvenile larynx-papilloma. The most important problem is an early diagnosis and prophylaxis of genital cancers in women. This was made possible by cytological and virological studies of cervical dysplasia. In the condylomatous and non-condylomatous lesions of the colli uteri virus particles have been found using the immunoperoxidase technique and immunserum against disrupted viral particles, i.e. against the common HPV antigen. However, the type of HPV can not be determined by this method. Using the same immunsera virus particles were found also in the bowenoid genital papules. The best model for human oncogenesis remains EV. The clinical and pathological morphology, virological and immunological studies on the non-specific and HPV-type specific humoral and cellular immunity are presented in detail.
D000818:Animals; D000917:Antibody Formation; D002417:Cattle; D002471:Cell Transformation, Neoplastic; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D027383:Papillomaviridae / Q000472:pathogenicity*; D011817:Rabbits; D014412:Tumor Virus Infections / Q000276:immunology / Q000473:pathology*; D002583:Uterine Cervical Neoplasms / Q000209:etiology; D014860:Warts / Q000209:etiology
Humane Papillomaviren und Onkogenese.