Historical perspectiveBeginning in the late 15th century, genital warts, and in fact many unexplained genital lesions, were attributed to an outbreak of syphilis occurring in Europe during the time [1]. Gonorrhea was later proposed as an etiology of genital warts. It was not until the discovery of the gonococcus in 1879 that this was refuted. The then new theory proposed that warts resulted from genital irritation caused by secretions 'disordered through venery', and led to the coining of the term venereal warts [1]. The viral etiology of skin warts was recognized in 1949 and it was not until 20 years later that viral particles were demonstrated microscopically in genital and anal warts [1].Rubin, in 1910, while examining histologic specimens from patients, noted abnormal cellular morphologic changes in clinically normal appearing tissue [2]. He proposed the concept that not only tissue invasion but also intrinsic cellular morphology could be determinants of neoplastic transformation [2]. The significance of lesions that were not invasive but were morphologically abnormal was hotly debated over the ensuing two decades until the concept of carcinoma in situ was introduced by Broder in 1932 [3]. The perfection and widespread use of the Papanicolao u (Pap) smear established the importance of these early lesions on a mass scale.
Structure and biology of human papillomavirusHuman papillomavirus (HPV), the etiologic agent of genital warts, is a nonenveloped DNA virus with an icosahedral capsid of 50-55 n in diameter containing 72 capsomeres [4]. The HPV genome exists in three forms within virions and infected cells: (1) a covalenfly closed circular supercoiled form; (2) an open circular form; and (3) a linear form [4]. All forms may exist as non-integrated plasmids in both benign and malignant lesions although DNA hybridization studies have also demonstrated integrated HPV genome within host cell nuclei. 103 Advances in Contraception. ISSN 0267-4874.