Papillomaviruses are double-stranded DNA viruses beloning to the Papillomavirus genus of the Papillomaviridae family. There exist above 200 types of HPV which, based on their tissue tropism, can be divided into cutaneous or mucosal categories. The link between HPV and malignancies is well-established, specifically with cancers involving the anogenital (cervical, vaginal, vulvar, penile, anal) tract and those involving the head and the neck. Epidemiologic studies indicate HPV infections as the major factors for the development of cervical cancer. Considering their association with the risk for cervical cancer, HPV types are classified as high-risk (HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68) and low-risk (6, 11, 40, 42, 43, 44, 53, 54, 61, 72, 73, and 81). An important role in the molecular pathogenesis of cervical cancer is played by the viral oncogenes E6 and E7 and their interaction with the p53 protein, that allows unchecked cellular cycling and has an anti-apoptotic effect, permitting the accumulation of chromosomal mutations without DNA repair. The retinoblastoma protein inhibits the effect of positive growth regulation and stopts cell growth, or it induces cell apoptosis in response to DNA damage. Progression to the malignant phenotype probably involves a genetic change in the pathways controlling intracellular or intercellular signaling. The chromosomal instability characterizing HPV infections may be one of the mechanism leading to these genetic modifications.
Keywords:- cancer prevention
- cervical cancer
- HPV infection
- screening programme.