Viruses in anogenital cancer.

Abstract

The association between sexual activity and cancer, first described in carcinoma of the cervix, has been expanded to include the majority of anogenital squamous epithelial carcinomas. Current evidence suggests that human papillomavirus (HPV) may be of great importance in the development of these tumours, whilst herpes simplex type 2 virus (HSV-2) and human immunodeficiency virus (HIV) may play minor roles. Certain types of HPV DNA, including types 16, 18, 31, 33 and 39 are found in most but not all anogenital cancers and pre-invasive neoplastic conditions. Viral genes E6 and E7 of HPV 16 and 18 are regularly expressed in HPV-positive tumours. In vitro, E6 and E7 genes have transforming properties which correlate with their ability to bind naturally occurring growth regulation proteins p53 and pRB. It has, however, become apparent that HPV alone does not provide the full aetiological explanation of sexually related carcinomas. The finding of latent, non-sexually-acquired HPV in a sizable proportion of the community, including children, has confounded simple theories of HPV transmission and cancer. Furthermore, in vitro experiments suggest that other factors may potentiate the effects of HPV. HSV-2 may possibly function as cofactor as it can synergize with HPV to cause transformation in vitro, and can transactivate HPV gene expression. HIV is associated with an increased rate of anogenital malignancies, particularly of the anus. Tumours in HIV-positive patients appear to have a worse prognosis, even before the onset of AIDS.