Epstein-Barr virus (EBV) infection contributes to the development of different types of human malignancies, especially nasopharyngeal carcinoma. As a herpesvirus, EBV can establish two major modes of virus-cell interactions: a latent or a lytic infection. Latent infection is prevalent in the vast majority of malignant cells in EBV-related malignancies. Inducing a switch from latent to lytic infection in a substantial fraction of malignant cells has long been considered as a potentially interesting therapeutic approach. Therapeutic benefits are expected from (1) the cytotoxic or cytostatic effects of viral products expressed in the context of the lytic cycle; (2) expression of viral enzymes capable of metabolizing pro-drugs selectively inside these cells and (3) broadening the expression spectrum of antigenic viral proteins. In this chapter, addressing non EBV-specialized readers, we first summarize the main aspects of EBV biology with emphasis on the cellular mechanisms known to control latent and lytic infections. Then, we outline the basic principles and requirements of cytolytic EBV activation performed with a therapeutic intent. Finally, we review the main categories of pharmacological agents reported to be active in the switch from latent to lytic infection, including drugs used for conventional anti-tumour chemotherapy, histone-deacetylase inhibitors and various miscellaneous compounds.
Part of the book: Herpesviridae