Cancer of the cervix is the third most common cancer among women worldwide, with incidence rates ranging from 3.8 per 100,000 women per year in Israel to 48.2 per 100,000 per year in Colombia. Epidemiologic and clinical data suggest that human papillomaviruses, especially HPV-16 and HPV-18, play the major role in the etiology of cervical cancer. However, many investigators acknowledge that HPV is neither necessary nor sufficient in the etiology of cervical cancer and that a multifactorial etiology is likely. HPV cannot be found in every patient with the disease and other factors, such as herpes simplex virus type 2 infection, cigarette smoking, vaginal douching, nutrition, and use of oral contraceptives, have been associated with cervical cancer. In two different animal models, tumors can be produced following exposure to DNA viruses and tars. Using those animal models as prototypes, we propose that the etiology of cervical cancer in humans could be an interaction between DNA viruses, specifically papillomavirus and/or HSV-2 infection, and tar exposure through cigarette smoking and/or tar-based vaginal douching.