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Cervical cancer is one of the most frequent diseases in women,it is comprises approximately 12% of all cancer in women worldwide and the second most common type, after breast cancer, with about 200,000 deaths annually and 500,000 new cases per annum. Persistent infection with one or more carcinogenic types of human papillomavirus (HPV) is an important etiologic factor in the development of cervical intraepithelial neoplasia and the progression to cervical cancer. HPV DNA has been detected in up to 99.7% of invasive cervical cancers worldwide.The carcinogenic effect of the "high-risk" HPVs, as defined by their documented association with invasive carcinomas, is thought to be mediated by two viral oncoprotein, E6 and E7, through their action of inactivating the function of two important cellular tumor suppressor, p53 and pRb. It has been demonstrated that the E6 oncoprotein interacts with p53 to promote its degradation, whereas the E7 oncoprotein form complex with Rb, leading to its functional inactivation as well as accelerated degradation. These synergistic effects result in a deregulated cell cycle control and are thus believed to be critically important in HPV-induced carcinogene