Abstract
Virally induced tumors provide the strongest case of host surveillance against neoplastic cells and their precursors. There is now substantial evidence that Epstein-Barr virus (EBV), hepatitis-B and C viruses (HBV and HCV), several types of papilloma viruses (HPV), Human Herpesvirus type 8 (HHV8) and human T-cell leukemia-lymphoma virus type I (HTLV I) and type II are responsible for approximately 15–20% of the total cancer incidence in the world. These viruses are widespread in populations where the associated diseases are seen at the highest incidence. In the vast majority of cases primary infection is either asymptomatic or is accompanied by benign proliferations of virus infected cells that often appear in concomitance with disturbances of the host immune responses and tend to regress spontaneously once full immunocompetence is restored. This, together with the observation that progression to malignancy occurs after long latency periods, and that the tumors are usually monoclonal, indicates that none of these viruses is by itself tumorigenic. An important aspect of viral oncogenesis is, therefore, the establishment of persistent asymptomatic infection where the transforming potential of the virus is controlled by a combination of cellular control mechanisms that regulate the expression of viral genes, and by strong immune responses that prevent the proliferation of virus infected cells.
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Masucci, M.G., Levitsky, V., Frisan, T., Levistkaya, J., De Campos-Lima, P.O. (1996). Virus induced cancer: The lesson of Epstein—Barr virus. In: Touraine, J.L., Traeger, J., Bétuel, H., Dubernard, J.M., Revillard, J.P., Dupuy, C. (eds) Cancer in Transplantation: Prevention and Treatment. Transplantation and Clinical Immunology, vol 27. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0175-9_19
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DOI: https://doi.org/10.1007/978-94-009-0175-9_19
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