Dual detection of human herpesvirus-6 and human papillomavirus type 16 and 18 in cervical carcinoma.

Introduction It is widely accepted that certain 'high risk' human papillomavirus (HPV) genotypes, particularly HPV 16 and 18 are aetiological agents in the development of neoplasia of the uterine cervix. The long latent period between initial HPV infection and emergence of carcinoma suggests that HPV alone is insufficient for malignant transformation and additional factors are required for the progression of HPV infected cells to a neoplastic phenotype. Cells with integrated HPV express viral E6 and E7 oncoproteins which are crucial for immortalisation of epithelial cells via their action on host p53 protein. It is therefore of particular interest to elucidate the molecular mechanisms that alter the expression of E6/E7 proteins during HPV-associated tumorigenesis. Recently, human herpesvirus-6 (HHV-6) has been shown to infect a HPV-immortalised cervical epithelial cell line and transactivate HPV 18 promoters, upregulating gene expression of E6 and E7 HPV oncoproteins (Chen et al., 1994; DiPaolo et al., 1994). HHV-6, first isolated from peripheral blood mononuclear cells of patients with AIDS and lymphoproliferative disorders, is the causative agent of exanthem subitum, heterophile-negative infectious mononucleosis and other febrile illnesses. HHV-6 has recently been detected in oral carcinomas (Yadav et al., 1994). HHV-6 also contains DNA sequences which can transform epithelial cells in culture.