The role of human papilloma virus in the molecular biology of cervical carcinogenesis.

Research exploring the E6-p53 and E7-pRb model has resulted in the identity of the viral gene's actions on numerous cellular proteins and processes normally involved in cell growth and proliferation. Specially, several findings have established the various ways by which the HPV-infected cell may escape controls governing cell growth and proliferation, including the fidelity of the host cell's genome and apoptosis. A large body of knowledge already generated in this area supports the view that high-risk HPV types have the ability to transform cells into a malignant phenotype. Such ability, however, is not sufficient to actually and inevitably produce cervical carcinoma, as indicated by the frequent spontaneous clearance of HPV infection and the long delay between the onset of persistent infection and emergence of the malignancy. Delay in the participation of cofactors has been suggested as explanation in this regard. However, it remains unclear how and when cofactors or factors that are innate in the HPV-infected cells launch the host cells into an irreversible progression to carcinoma.