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Human Papillomavirus (HPV) are epitheliotropic for stratified malpighian epithelia such as those of the cervix, vulva or anal canal. Mucosal papillomaviruses are responsible for several clinical lesions and can be classified as non oncogenic and oncogenic viruses. The first ones are responsible for benign lesions such as external genital warts (EGW) or condyloma due to HPV 6 and 11. The second ones include oncogenic viruses such as HPV 16 and 18, the most common ones, and HPV 45, 31, 33, 52 etc which are involved in invasive cancers preceded by cervical, vulvar, penile or anal intraepithelial neoplasia. Oncogenic HPV are detectable in 99.7% of cervical cancers (Bosch et al, 1995). Cellular immunity plays a key role in controlling and killing infected or transformed keratinocytes. Nevertheless, around 10% of women having infected cervical mucosa are not able to control oncogenic HPV and develop cervical intraepithelial neoplasia (CIN). High grade CIN (CIN3) require surgical treatment before their progression to invasive cancers in 30% of cases (McCredie et al, 2008; Ostor et al, 1993). A great priority is then to develop a preventive vaccine to protect against HPV infection. In women with CIN, therapeutic vaccine could be used to eliminate previously infected or transformed keratinocytes and avoid surgical treatment.

Current Insight into Anti-HPV Immune Responses and Lessons for Prophylactic and Therapeutic Vaccines