Abstract
HPV has been identified as the major aetiological factor in cervical carcinogenesis,1 being detected in 90–100% of cervical cancer specimens compared with 20% of controls.2 In addition, the HPV viral genome has been identified in most of the precursor lesions of cervical intraepithelial neoplasia.3 HPVs are epitheliotropic and were thought to preferentially infect squamous epithelia only. However, it is now known that much of the virus is present at the squamo–columnar junction. Moreover, a consistent, strong and robust association between infection by high-risk HPV types and risk of development of adenocarcinoma of the cervix has been demonstrated.4 5