RESUMEN
The nature of the interaction between papillomaviruses (PV) and their infected host has led to the identification of ways in which the viral oncoproteins can transform the infected host cells into cancer cells. As viral persistence is required for malignancy, and persistence requires avoidance of immune attack by the host, defining the relationship between PV and the immune system is also paramount in understanding tumorigenesis. It has emerged that PV have evolved several ways in which to prevent clearance by the host immune system. The limitation of the PV replication cycle to the epithelium, together with low level expression of the virus proteins and an absence of inflammation, minimises the exposure of virus to immune cells. In addition, more recently it has been shown that, like many other viruses, PV can directly subvert the immune response, including interference with the interferon pathway, modulation of antigen presentation, inhibition of interleukin-18 activity and down-regulation of major histocompatibility class I on infected cells. Collectively these mechanisms explain how PV lesions are able to persist for long periods of time in immunocompetent hosts.