Introduction

Extraordinary developments have occurred since molecular and epidemiological tools have proven that oncogenic human papillomaviruses (HPVs) cause virtually all cervical cancers, as well as a proportion of other anogenital cancers (vulvar, vaginal, anal, penile) and some oropharyngeal cancers (particularly tonsillar).1 2 In addition, low-risk HPV types 6 and 11 are the causative agents of the majority of genital warts,3 a benign but very common sexually transmitted disease, estimated to occur in up to 10% of the population4 and with an estimated annual burden of new cases worldwide of 30 million.

With the development of viral-like particles and the relatively short translation to phase 3 clinical vaccine trials showing that prophylactic HPV vaccines targeting the two most common causes of cervix cancer, HPV 16 and 18, are safe, immunogenic and efficacious,5–7 we now observe the outcome of these vaccines implemented as public health tools in those countries that can afford such programmes. Where coverage has been high to the appropriate target population, reduction in disease has already been seen for those HPV-related diseases with the shortest incubation periods. For example, in Australia the quadrivalent HPV (6, 11, 16, 18) vaccine was started in April 2007 in a comprehensive, national, government-funded, school-based, ongoing programme for girls 12 years of age, with a catch-up program to 26 years of age until December 2009. In this real-life situation, a statistically significant reduction has already been reported in genital warts of almost 60% in young women of vaccine-eligible age.8 These findings are most likely related to the catch-up component of the programme, rather than the school-based programme. However, with time and continued good vaccine coverage, one would expect a change in sexual …