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Significance Epstein-Barr virus (EBV) efficiently transforms human B cells and causes B cell lymphomagenesis especially in immunocompromised patients. We study this process in genetically engineered mice to untangle the interplay of EBV oncogenes. We find Epstein-Barr nuclear antigen (EBNA) 3A to have both oncogenic and tumor suppressive roles. First, EBNA3A promotes B cell transformation by inhibiting LMP-driven plasma cell differentiation, a function which can be mimicked by aberrant activation of early B cell factor 1 (EBF1). Second, EBNA3A blunts Myc-driven proliferation, rendering B cell transformation dependent on Myc activation by the EBV protein EBNA2. The presented mouse model thus highlights the role of EBV oncogenes in orchestrating B cell transformation through control of B cell differentiation and Myc levels.

Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell lymphomagenesis