The link between genital high-risk Human papillomavirus (HPV) infections and CC was first demonstrated in the early 1980s by Harold zur Hausen, a German virologist. (Gissmann, L et al, 1983) HPV infection may be transient or persistent. When it persists, HPV induces changes in cells of the cervix, precisely in the transformation zone. These changes constitute the precursor lesions of cervical cancer. These precursor lesions are either called precancerous lesions, dysplasia or cervical intraepithelial neoplasia (CIN). Left untreated, they can progress from mild (CIN1) to moderate (CIN 2) to severe (CIN 3) dysplasia, and then to cancer. It appears that dysplasia is asymptomatic and progresses to cancer over a prolonged period of time, usually 7 to 20 years.