Epstein-Barr virus (EBV) is able to override the mechanisms that normally regulate the proliferation of human B-lymphocytes. In the absence of other extracellular signals, EBV infects resting B-lymphocytes and drives the infected cells into the cell-division cycle. Recently, there has been much interest in defining the molecular mechanisms by which EBV reprograms the cell cycle control machinery in B-lympho-cytes (1 –19 ).