Epstein-Barr virus (EBV) is implicated in the pathogenesis of a number of human lymphoid malignancies, including the immunoblastic B lymphomas that arise in immunocompromised individuals, Burkitt's lymphoma, Hodgkin's disease, and certain T cell lymphomas. The immunoblastic lymphomas are most likely a direct consequence of EBV-driven B cell lymphoproliferation that would in normal circumstances be eliminated by virus-specific cell-mediated immune responses. The other EBV-associated malignancies arise in individuals with more or less intact cellular immune responses and appear to have a complex multi-step pathogenesis. Throughout the EBV-positive lymphoid malignancies there is an intimate association between tumour cell phenotype and virus latent gene expression, with each of the three forms of latency seen in in vitro models being exemplified in vivo. Tumours with these different forms of virus latency will differ in their susceptibility to EBV-specific immune T cell control.