Available data indicate that cervical cancer develops through infection to preinvasive lesions to invasive cancer, a process that on average takes decades[8]. However, the molecular mechanisms involved in the development of a persistent HPV infection resulting in the development of cervical cancer are not well-established. Host innate immunity and adaptive immune response all are responsible for the regression, persistence, or progression of HPV infection. For example, a polarization of the immune response for T-helper 2 (Th2) was observed in women with HPV infections that evolve into high-grade lesions[9], whereas squamous intraepithelial lesions and in situ carcinomas evading immunological control seem to be influenced by the cellular antigen presentation system and the HLA receptors[5]. The transcriptional blockage of the HPV DNA also facilitates the malignant transformation caused by HPV persistent infection, and in this case, the tumor necrosis factor-α (TNF-α)-mediated cascade plays an important role[5].