Background

Human papillomavirus (HPV) is the most common viral sexually transmitted infection, with estimates that up to 75 per cent of people are infected at some time.1 Whilst most infection resolves without symp-toms, some human papillomavirus infections can persist and cause cancer. In particular, the role of HPV infection in causing cervical cancer, the second most common cause of cancer in women worldwide, is undisputed. HPV exists as over 200 types but only some of these types are oncogenic (causing cervical, other anogenital cancers, oral and laryngeal cancers.) Other common HPV types cause skin warts. The recent development of vaccines to protect against infection with oncogenic HPV types holds promise for the primary prevention of both cervical cancer and its precursors. The vaccines are based upon the Australian discovery that the major HPV capsid protein L1 can self assemble into virus-like particles (VLPs) when independently expressed in cultured cells,2 and induce high titres of type-specifi c and protective neutralising antibodies in animals. These VLPs lack any viral genetic information and are not infectious. VLP based vaccines against the cancer causing HPV types 16 and 18, and against types 6 and 11 (which cause genital warts) are in current clinical trials. Early results are promising, with vaccine providing 100 per cent protection (95 % CI 90-100%) against persistent infection with HPV 16.3 These vaccines are likely to become available in the next few years. According to a recent meta-analysis of worldwide prevalence data, vaccinating against HPV 16 and HPV 18 could pre-vent over 70 per cent of invasive cervical cancers worldwide.4 Human papillomavirus research meeting objectives With a view to initiating discussion and research into the possible future role of HPV vaccines i