HUMAN PAPILLOMAVIRUSES (HPV) are ubiquitous viruses causing papilloma on the skin and mucosal surfaces. Sexual transmission is the usual way of spreading genital papilloma, also called condyloma.(1) To date, more than 100 different HPV types have been defined on the basis of DNA homology. About 40 of these are associated with anogenital mucosal infection leading to condyloma and cancer.(2,3) Cervical cancer is one of the most important causes of death among women worldwide. About half a million new cases are detected every year. Many studies about cervical cancer etiology have demonstrated risk factors including sexual and reproductive behavior, socioeconomic status, cigarette smoking, oral contraceptive use, diet, and influence of female sexual hormones.(4,5) Collectively, epidemiologic evidence from an extensive World Health Organization study in 22 countries has concluded: HPV infection is an essential cause of cervical cancer.(3) Several reports have demonstrated a high incidence and a close relation between cervical cancer and HPV DNA especially of high-risk HPV being found in more than 90% of all squamous cell carcinomas from the anogenital tract.(6,7) Most clinical lesions of the cervix can be detected by Papani-colau (Pap) smears, tissue biopsies, or by colposcopic examination.(7) Serological assays using HPV-like particles have been recently developed to detect specific HPV antibodies in HPV-infected women. Until now, polymerase chain reaction using consensus primers is the most sensitive DNA detection method to reveal infection in precancerous and cancerous cervical lesions.(6,7) Thus, HPV has been subdivided into 3 risk groups: low-risk HPV types (e.g., in condylomata acuminata and light dysplasia cases), whereas high-risk HPV types have been detected in dysplastic tissues and carcinomas at high frequency.(8) The risk of malignant transformation for intermediate HPV types has not been definitively elucidated.