Regulation of the latent-lytic switch in Epstein-Barr virus
Shannon C Kenney1, Janet E Mertz2
1McArdle Laboratory for Cancer Research, 1400 University Avenue, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA; Department of Oncology, 1400 University Avenue, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA; Department of Medicine, 1400 University Avenue, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA.
Abstract:
Epstein-Barr virus (EBV) infection contributes to the development of several different types of human malignancy, including Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. As a herpesvirus, EBV can establish latent or lytic infection in cells. EBV-positive tumors are composed almost exclusively of cells with latent EBV infection. Strategies for inducing the lytic form of EBV infection in tumor cells are being investigated as a potential therapy for EBV-positive tumors. In this article, we review how cellular and viral proteins regulate the latent-lytic EBV switch in infected B cells and epithelial cells, and discuss how harnessing lytic viral reactivation might be used therapeutically.
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