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Abstract
A small number of fundamental cell signaling pathways are key to the regulation of proliferation and differentiation responses during normal development. Two of these pathways, the Notch and Wnt pathways, have proven to be attractive targets for virus interaction and manipulation. In general, viral gene expression and replication are intimately linked to the differentiation state of the infected cell and, in the case of the gamma herpesviruses, establishment of a lifelong persistent infection in the host is also dependent on the proliferative expansion of an infected B cell population. This review examines the ways in which the gamma herpesviruses Epstein-Barr virus (EBV) and Kaposi’s sarcoma–associated herpesvirus (KSHV) have exploited the Notch and Wnt pathways to advance their own life cycles. The virus-pathway interactions are compared with the mechanisms and outcome of cellular Notch and Wnt signaling.
