Human papillomavirus (HPV) infections involved in the neoplastic process of the uterine cervix as established by prospective follow-up of 513 women for two years.
A total of 513 women with cervical HPV infections have been followed-up since 1981 (mean 25.6 months) to establish the biological potential of HPV in cervical carcinogenesis. On each attendance, the patients were subjected to colposcopy accompanied by Papanicolaou (PAP) smears and/or punch biopsies. The latter were analysed for HPV particles on TEM, for the cytopathic changes of HPV, as well as for HPV structural proteins. The local immunocompetent cell (ICC) infiltrates are enumerated using ANAE-technique to define B-, MPS- and T cells, and monoclonal antibodies for T cell subsets, NK and K cells and Langerhans cells. HPV DNA typing was accomplished by Southern blot and spot hybridization using the DNA probes for HPV 6, 11, 16 and 18. Antibody titres for HSV were measured, and Chlamydia trachomatis isolations completed in cervical swabs. No correlation with the clinical course, e.g. regression (RE), persistence (PE), progression (PR) or recurrence (RC) of the HPV lesions could be established for the following factors; expression of HPV antigens, presence of HPV particles on TEM, Chlamydia in cervical swabs, the levels of HSV antibodies, and the levels of the ICCs. The OKT4+/OKT8+ cell ratio, however, was inversely correlated with PR, being most markedly reduced in recurrent lesions. Of the 513 lesions, 24.8% regressed, 59.8% remained persistent, and 14.1% progressed, 11.9% having been coned due to progression into CIS. So far, 1.1% of lesions have recurred after such a treatment. The progression rate was highest (45.5%) in HPV 16 lesions, followed by that (27.3%) in HPV 18 lesions, as contrasted to 0% and 13.3% for HPV 6 and 11, respectively. The results clearly confirm that cervical HPV infections are capable of progressing into CIS and thus show a natural history equivalent to that of classical CIN. The inherent potential of HPV 16 and HPV 18 lesions for clinical progression was clearly established, supporting the concept on HPV 16 and HPV 18 as the high risk HPV types in cervical carcinogenesis.
D000293:Adolescent; D000328:Adult; D000368:Aged; D001707:Biopsy, Needle; D004273:DNA, Neoplasm; D004279:DNA, Viral / Q000235:genetics; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008875:Middle Aged; D027383:Papillomaviridae / Q000235:genetics; D010641:Phenotype; D011446:Prospective Studies; D014412:Tumor Virus Infections / Q000150:complications* / Q000276:immunology / Q000473:pathology; D002583:Uterine Cervical Neoplasms / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D014764:Viral Proteins
D004273:DNA, Neoplasm; D004279:DNA, Viral; D014764:Viral Proteins