Strong evidence indicates genital human papillomavirus (HPV) infection as a key factor in cervical cancer and pre-cancer development. The specific role of HPV in cervical neoplasia has not been established and no studies to date have examined the natural history of HPV from infection to neoplasia. Studies documenting the presence of HPV DNA in disease-free women suggest that cofactors are required by HPV for neoplasia to occur. These cofactors may include C.trachomatous, herpes simplex virus infection, oral contraception use, cigarette smoking and cervical immaturity. The latter is probably related to squamous metaplasia, the target epithelium where neoplasia occurs.
The specific aims are: 1) to observe the natural history of HPV and 2) to determine risk factors related to the development of cervical neoplasia in adolescents. This population was chosen for several reasons. First, adolescents with HPV and limited years of sexual activity are ore representative of an early infection (short exposure time) than most adult populations who have been sexually active for numerous years. Second, since rates of neoplasia are increasing in younger women, cofactors identified in this group may represent important factors for the acceleration of neoplastic development. Last, adolescence is marked as a time of abundant metaplastic activity, representing an ideal population to study the role of cervical immaturity in neoplasia. Females aged 13-18 years and positive for HPV DNA will be asked to undergo a colposcopic examination and face-to-face interview. Those females sexually active less than two years with a positive HPV DNA test and no evidence of cervical neoplasia will be asked to enroll in a longitudinal study. Patients will be examined at the initial visit and every four months or until CIN develops. Colposcopic examinations, cytology, test for sexually transmitted diseases and face-to-face interviews for information on sexual behaviors, contraceptive use, and cigarette and substance us will be performed at scheduled intervals. This study will describe the natural history of latent HPV infection and calculate risk factors for the accelerated development of CIN in a case-control and cohort population. The results from this study will be related to the prevention and education of pre-cancer lesions in young women as well as identifying a clinical model for the role of viruses in abnormal cellular development.
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