| Popis: |
Specific types of human papillomaviruses (HPVs) (mostly HPV-16, HPV-18) are etiologically involved in the development of cervical cancer (1,2). Although viral DNA induces immortalization of primary human keratinocytes in vitro, infection alone is not sufficient to cause malignant transformation (3,4). In agreement with the multihit concept of many human neoplasias, additional damaging events are required to convert a cell toward malignancy and to induce cervical cancer (5,6). Furthermore, the course of the disease is not only the result of failing intracellular surveillance mechanisms (5,7), but is also determined by the immune status of the infected individual (8,9). Epidemiologic studies have demonstrated that immunosuppressed patients or persons with impaired immunocompetence have a higher virus susceptibility and virus spread, and an increased incidence of preneoplastic lesions than age-matched controls (9). |
