Molecular Mechanism Potential Targets for Blocking HPV Induced Lesion Development

Abstract

Persistent infection with high risk HPV is the etiologic agent associated with the development of cervical cancer (CC) development. However, environmental, social, epidemiological, genetic, host factors may have a joint influence on the risk of disease progression. Cervical lesions caused by HPV infection can be removed naturally by the host immune response only a small percentage may progress to cancer; thus, the immune response is essential for the control of precursor lesions CC. We present a review of recent research on the molecular mechanisms that allow HPV infected cells to evade immune surveillance potential targets of molecular therapy to inhibit tumor immune escape.