Cervical cancer encompasses both squamous-cell carcinoma and adenocarcinoma, which are thought to have different cellular origins (1–3). Unlike most cancers, the development of cervical cancer is intrinsically linked to infection by a very common virus (4,5). This is the human papillomavirus (HPV), which is a small non-enveloped icosohedral particle containing a double-stranded circle (or episome) of DNA (6). Papillomaviruses typically contain around 8000 base pairs of DNA and usually encode eight or nine open reading frames (or genes) and with these they complete their productive life cycle in the epithelium or cause neoplasia and possibly cancer (3,7). At the outset, there are two very important points to note regarding these viruses. The first is that although there are a large number of different papillomavirus types that infect humans, only a small subset (known as the “high-risk” types) cause lesions which progress to cancer (4,8). These viruses, like all papillomaviruses, are prevalent in the general population, which leads us to the second point. Only a small fraction of these high-risk papillomavirus infections will progress to cancer (8,9). Most will be cleared by the body's immune system over a period of months or years. Thus the development of cervical cancer is associated with persistent infection by a high-risk HPV type. In fact, this is not quite the whole story, as HPV-associated cancers develop primarily at certain sites of the body, and the most important of these is the cervical transformation zone, although other transformation zone sites are also vulnerable, such as the anal transformation zone (2,3). These are particular sites where viral gene expression is not always properly regulated and where the expression of viral genes can, over time, facilitate the accumulation of genetic errors in the infected cell that can ultimately lead to cancer.