Cancer of the uterine cervix and human papillomavirus infection

Human papillomaviruses (HPVs) have emerged as the principal sexually transm itted causal agents in the development of cancer of the uterine cervix in w omen. They also cause a variety of benign lesions, warts, intraepithelial n eoplasia and anogenital, oral and pharyngeal papillomas, Presently, more th an 100 HPV genotypes have been identified in humans, and about one-third of them have been sequenced. Of these, while HPV types 16 and 18 are consider ed to be the high-risk types, BPV 6 and 11 are the low-risk types in the de velopment of cervical cancer. Evidence for causal role of BPV in the develo pment of cervical neoplasia comes from the etiological and epidemiological observations together with the experimental findings of the molecular pathw ays elicited by HPV-transforming genes. Further evidence in favour of papil lomavirus as the carcinoma virus comes from the findings of presence of HPV infections in cancers of oral, esophageal, larynx and non-melanoma skin ca ncers. The oncogenic potentials of the virus have been attributed to its E6 and E7 genes. The products of these two genes stimulate cell proliferation by activating the cell-cycle-specific proteins and interfere with the func tions of cellular growth-regulatory proteins, p53 and Rb. Identification an d characterization of several human pathogenic HPV types warrant prevention of viral infection through vaccination or therapeutic intervention which c ould eventually control infection and expression of human pathogenic papill omaviruses.