[Human papillomavirus infection. Pathology and molecular pathology]

Cervical cancer is the second most frequent female malignoma worldwide and accounts for about 500,000 cases every year. The peak incidence lies between 35 and 55 years of age. Persistent infections with a group of 15 so-called high-risk human papillomaviruses (HR-HPV) are the cause of cervical carcinogenesis of squamous cell carcinomas and for most of the adenocarcinomas. The transforming potential of HR-HPVs is based on the interaction of viral oncogene products E6 and E7 with the cellular tumor suppressor proteins p53 and pRB. The resulting loss of cell cycle control sets the basis for additional, as yet only incompletely discovered, genetic and epigenetic changes, finally leading to invasive growth. Preneoplastic changes, cervical intraepithelial neoplasias, can be identified morphologically, thus allowing for therapeutic interventions. Since November 2007, the Ständige Impfkommission, the German standing committee on immunizations, has recommended the prophylactic use of vaccines against the two most frequent HR-HPV genotypes, HPV-16 and HPV-18, in women age 12-17 years before first sexual intercourse. In addition to cervical cancer, HPV infections are responsible for the development of genital warts (condyloma) and a number of vaginal, vulvar, and anal intraepithelial neoplasias. HPV infections are usually transmitted sexually.