The Epstein-Barr virus (EBV) infects most of the world's adult population. In most cases primary infection and virus persistence are asymptomatic, the virus having evolved a sophisticated strategy to exist long-term in the B cell pool. However, EBV can contribute to the development of several human B-cell lymphomas, which include Hodgkin's lymphoma (HL), Burkitt's lymphoma, and a subset of diffuse large B cell lymphomas. EBV potently transforms resting B cells in vitro (Young & Murray, 2003; Young & Rickinson, 2004; Oyama et al., 2003; Oyama et al., 2007). Two questions central to our understanding of the origins of EBV-associated B cell lymphomas are; 1) how the host and virus interact to allow benign persistent latent infection, and 2) how perturbation of this normal homeostasis leads to neoplastic transformation. This review will summarise current knowledge of how the EBV life cycle is regulated in the B cells of the asymptomatic host. It will also discuss how the disruption of normal B cell homeostasis can contribute to the development of B cell lymphomas, focussing on several novel pathogenic mechanisms in EBV-associated HL which include the suppression of the virus lytic cycle and the activation of collagen receptor signalling.