During the past decades it became evident that at least 21% of the global cancer incidence is linked to viral, bacterial and parasitic infections. Among these infectious agents, viruses play a rather dominant role. In part we do understand the mechanisms by which these agents contribute to cancer development. Some of them act as direct carcinogens, inserting specific genes or complete genomes into the respective host cells. In initial stages of infections they persist in a latent form. This latency appears to be controlled by host cell signalling cascades. Cancer development only occurs after genetic or epigenetic modification of cellular controlling genes, affecting the function of the respective signalling cascades. These modifications are either due to pre-existing mutations in the germ line or to events affecting the respective cells during lifetime.
A second mode of carcinogenesis is mediated indirectly, either by immunosuppression, frequently activating other latent tumorviruses or by the induction of oxygen or nitrogen radicals. Types of infection, latency periods, mechanistic aspects and prevention of cancers linked to infections will be discussed. In addition, reasons will be analyzed to suspect additional human cancers, not yet associated with infections, to be caused by such events.
