Introduction

Cervical cancer is the second commonest female cancer worldwide. Over the last few years, the evidence that sexually transmitted human papillomavirus (HPV) infection is involved in the development of most cases of cervical cancer has become virtually conclusive (Howley 1991, Schiffman 1992). HPV is therefore among the most important targets for practical cancer prevention. Screening for HPV is cheap and reliable, and animal studies suggest that vaccination may prove effective both in curing established infection and in preventing re-infection (Campo et al. 1993).

Against this background, formal modelling of the transmission and persistence of HPV infection would be a useful next step towards understanding the epidemic. The data required for preliminary simple models are beginning to emerge from case-control and prospective studies, but it is already clear that the natural history of infection is complex and heterogeneous. Statistical models of the natural history of various chronic diseases are reviewed by Gore (this volume). As for HIV, HPV susceptibility and infectiousness may be significantly influenced by other sexually transmitted infections as well as by genetic and immunological host factors.

The aim of this paper is to summarise the evidence that HPV is the cause of most cervical cancers, and to indicate what data should now be collected to elucidate its transmission dynamics. There have been rapid advances over the last few years in HPV diagnostic methods and our understanding of the relationship between HPV, dysplasia and malignancy. Much of the material summarised below is described in the recent IARC Scientific Report entitled The Epidemiology of HPV and Cervical Cancer (IARC 1992).