The question of whether human papillomavirus (HPV) infection causes, or at least contributes to, the development of cervical carcinoma has been a topic of much scrutiny and controversy over the past few years. The sexual mode of transmission of genital HPVs and detection of viral DNA in cervical tumors suggest a causal role at some stage during malignant progression. To some extent it seems that the epidemiological data accumulated so far have served to confuse as much as to clarify the issue, and the distribution of genital HPVs in the general population appears to be more complex than originally anticipated. However, experimental systems that have been used to study HPVs, in particular recent studies utilizing human genital epithelial cells, have provided strong evidence that certain HPV types can cause premalignant changes in these cells. The development of cervical cancer is a multistage process, and HPV infection alone is clearly not sufficient for full malignant transformation. Nevertheless, identification and control of HPV infection may be of critical importance in the diagnosis and treatment of this disease.