Cancer arises from accumulation of changes in cells that result in a loss of the control mechanisms which govern normal cell proliferation or survival. Certain persistent viral or bacterial infections can promote this chain of events by interfering with the regulation of cell proliferation or cell death or by inducing DNA damage that promotes the accumulation of genetic changes. The infectious agents that have been recognised as human carcinogens include the viruses EBV, KSHV, HPV, HTLV-I, Hepatitis B virus (HBV), Hepatitis C virus (HCV) and the bacterium Helicobacter pylori, About 17% of cancer cases world-wide are associated with these infectious agents, resulting in 1.6 million newly diagnosed cases of cancer annually. The molecular differences between cancer cells and normal cells are very subtle with the consequence that current cancer treatments have many side-effects on normal cells and toxicity in patients. The role of an infectious in the cancer development may provide unique therapeutic targets or approaches to the treatment of those cancers. A feature common to all oncogenic infectious agents is their long term persistence in infected individuals. Interfering with the persistence represents one of the most appealing options for preventing infection-associated cancer. Vaccines against HPV and HBV now licensed for use will eventually prevent many of the cancers associated with those agents but it will be many years before the effects feed through into reduced cancer incidence. Apart from the treatment of H. pylori infections using antibiotics, it is not currently possible to eradicate already established persistent infections with the oncogenic viruses or bacteria. In spite of the wide distribution of most human oncogenic viruses or bacteria, infection-associated cancer only occurs in comparatively few infected individuals. There is therefore a need for methods to identify infected individuals who are at a higher risk of progression to malignant disease.