Epstein-Barr virus infection and the pathogenesis of malignant lymphomas.

EBV is associated with an ever increasing number of human malignancies, which illustrates the importance of understanding how the virus contributes to tumorigenesis. Recent work has identified as set of EBV latent proteins that are indispensable for B cell transformation in vitro, and possible mechanisms of action are beginning to emerge for some of these proteins. In addition to viral gene expression, host factors appear to be involved in the development of virus associated tumours. Firstly, virus specific immunity is important for preventing the outgrowth of EBV associated tumours. Disturbances of EBV specific immunosurveillance can occur as a consequence of systemic immunosuppression or due to local factors, some of which may directly or indirectly result from the expression of EBV genes. Secondly, the phenotype of virus infected cells seems to be important. Thus, many EBV associated tumours appear to arise from cell types that do not represent a "physiological" target for the virus and thus may not be adapted to establishing asymptomatic persistent EBV infection. Furthermore, the function of transformation associated viral gene products may vary according to the cellular phenotype.