Human papilloma virus (HPV) infections related to cervical intraepithelial neoplasia (CIN) and squamous cell carcinoma of the uterine cervix.
Human papilloma viruses (HPV) consist of a heterogenic group of viruses (32 different HPV types identified to date) known to induce a variety of squamous cell tumours (papillomas and warts) in the skin, and on mucous membranes of respiratory, gastrointestinal and genitourinary tracts. In the genital tract, the venereal wart (Condyloma acuminatum) has been recognized since ancient times, and known to be a sexually transmitted disease (STD). In 1976, two other morphologically distinct HPV lesions were described in the uterine cervix, known currently as a flat and an inverted condyloma. Subsequently, these new HPV lesions were shown to be frequently associated with concomitant cervical intraepithelial neoplasia (CIN) and carcinoma in situ (CIS) lesions, and occasionally with invasive cervical carcinomas as well. These morphological findings, substantiated by the increasing number of reports of malignant transformation of HPV lesions, as well as data from animal experiments and epidemiological surveys, have lent support to the concept that HPV might be involved in the development of cervical (and other) human squamous cell carcinomas. Further evidence has been provided by the recent discoveries of HPV structural proteins (viral antigens) and HPV type 11 DNA in lesions of CIN, as well as HPV 16 and 18 DNA predominantly in invasive cervical carcinomas. So far, HPV 16 and HPV 18 are the only HPV types with DNA shown to exist integrated in the host cell DNA. At present, cervical (and other) HPV lesions are the subject of intense study utilizing epidemiological, morphological, immunohistochemical, biochemical and molecular biological methods (recombinant gene technology) to provide further evidence of the suggested causal relationship between HPV and cancer. Prospective follow-up studies are also in progress to explore the natural history of cervical HPV lesions as well as the factors (immunological, epidemiological, synergistic actions, etc.) which modify it. Despite the rapid progress made in papilloma virus research in the last few years, many important questions have still to be answered before the final conclusions can be drawn as to the possible role of HPV in cervical carcinogenesis.
D000818:Animals; D002294:Carcinoma, Squamous Cell / Q000209:etiology* / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000473:pathology; D004247:DNA / Q000032:analysis; D004273:DNA, Neoplasm / Q000032:analysis; D005260:Female; D006801:Humans; D009693:Nucleic Acid Hybridization; D027383:Papillomaviridae / Q000502:physiology; D014412:Tumor Virus Infections / Q000150:complications* / Q000453:epidemiology / Q000276:immunology / Q000473:pathology; D002583:Uterine Cervical Neoplasms / Q000209:etiology* / Q000473:pathology; D014779:Virus Replication
D004273:DNA, Neoplasm; D004247:DNA