The Human Papillomavirus (HPV) etiology of cervical carcinoma was first proposed in the 1970’s and it was soon clear that HPV infections were the most important risk factor for this cancer [–3]. By the late 1990’s, epidemiologic, virologic and molecular studies from all over the world established that all cervical cancers were the end result of a process that was initiated by sexually transmitted infections by a group of high-risk (cancer-causing) HPVs [–9]. Initially, the prospects of developing prophylactic HPV vaccination against a sexually transmitted infection did not appear to be very high. However, animal studies showed that papillomavirus-based vaccines protected rabbits, dogs and cattle against their respective papillomavirus–induced diseases [10,11]. This led to the development of HPV vaccines based on the major viral protein which when expressed, self-assembles into virus-like particles . Because HPV-16 and 18 are found in almost all cervical cancers, cancer prevention appeared to be within reach.