Genital warts and cervical cancer. II. Is human papillomavirus infection the trigger to cervical carcinogenesis?
Evidence of a biologically significant association between subclinical papillomavirus infection (SPI) and cervical neoplasia raises the question of whether this is a causal relationship. Human papillomavirus (HPV) infection of metaplastic epithelium in the cervical transformation zone is relatively common, producing latent infection in susceptible persons. The epidemiological characteristics of SPI and cervical cancer are essentially identical and there is a strong clinico-pathological association between condylomas and anogenital carcinoma. Tissue culture cells have been transformed from a normal to a neoplastic phenotype by animal papillomaviruses, and there is preliminary data reporting upon the successful identification of HPV genomic sequences in tumor cells. SPI commonly coexists with foci of cervical intraepithelial neoplasia (CIN). Areas of apparent transition are seen, and these two lesions are linked by a discernible spectrum of morphologic change. Such circumstantial evidence gives biological plausibility to the suggestion that HPV may be a cervical carcinogen. It is postulated that cervical neoplasia arises by progression from benign viral hyperplasia, through varying stages of koilocytotic atypia with associated dysplasia, to unremarkable carcinoma in situ. Invasion is presumed to reflect the emergence of an aggressive heteroploid clone, an age-related decline in host immune surveillance or an interaction of both factors.
D000818:Animals; D002278:Carcinoma in Situ / Q000209:etiology*; D005260:Female; D006801:Humans; D027383:Papillomaviridae; D014412:Tumor Virus Infections / Q000150:complications* / Q000473:pathology; D002583:Uterine Cervical Neoplasms / Q000209:etiology*; D014860:Warts / Q000150:complications*