A Research For Malignant Transformation Of Human Papillomavirus Type 16-immortalized Human Cervical Epithelial Cell By Defined Cloned DNA Fragments Of Herpes Simplex Virus Type 2

Human papillomaviruses (HPVs and herpes simplex virus type 2 (HSV-2), both of which are oncogenic DNA viruses spread primarily by sexual contact, are closely associated with human cervical cancer. It is now known that the high-oncogenic-risk HPV types, especially HPV16 and 18, are the principal etiologic agents for cervical cancer. However, the development of cervical cancer is a multistep process that can't be explained simply by infection with specific types of HPV. Progression to the malignant phenotype after HPV infection in vivo apparently requires additional cofactors. Recent epidemiological evidence indicates that women infected with HSV-2 and HPV16 or 18 are at greater risk with respect to cervical cancer compared to woman infected with only one virus. This suggest that high-oncogenic-risk HPV and HSV-2 can be cofactors during the development of cervical cancer. In order to assess the hypothesis that HSV-2 cooperate with the high-oncogenic-risk HPV to produce a malignant phenotype. In this study, we investigated the transforming effects of HSV-2 DNA fragments on HPV16-immortalized human cervical epithelial cells, and furthermore investigated the transforming mechanism.