The impact of Human papilloma virus (HPV) infection on the development of cervical neoplasia

The genesis of uterine cervix carcinoma has as central etiology the active infection of human papilloma virus (HPV), especially high oncogenic risk subtypes. However, this is a necessary, but not sufficient cause of virtually all cases of cervical cancer worldwide. At present, the proportion of cervical carcinomas attributed to HPV infection is estimated at 99%. It is considered that the pathogenesis of cervical carcinoma is the result of the proliferation of one or, at most, a few HPV-infected cells. Invasive cervical cancer arises in cervical intraepithelial neoplasia, which in turn develops preferentially in squamous metaplasia of certain limited areas. These areas represent the most important morphologic characteristic in cervical intraepithelial neoplasia. It is still unknown the precise mechanism for the development of separate fields in HPV-related intraepithelial neoplasia and the variable susceptibility of reserve cells for different HPV genotypes. The goal of any cervical cancer screening test is to identify women who are at risk of cervical cancer development and to reassure others that do not belong to this category. Cervical cytology (Pap smears) were the primary screening tests. More recently, carcinogenic HPV DNA testing has been included as adjunctive test or as a primary screening test based on the central role of carcinogenic HPV infection in the development of cervical cancer. New biomarkers, including those that measure the interaction of host and virus, are being considered either as stand-alone molecular assays or in conjunction with cytology or carcinogenic HPV DNA testing to improve its sensitivity or specificity, respectively. .Profilactic HPV vaccination of women who are sexually active may provide protection against HPV-16 or HPV-18 infection which may lead to cytological abnormalities, precancer or cancer.