Specifically, genesinvolved in proliferation and the DDR, including ATM/p53-dependent targets(Elkon et al., 2005), were highlyinduced early after infection and then attenuated during the transition to LCL.We propose that aberrant induction of cellular DNA replication early after EBVinfection activates a DNA damage response that is dependent on EBNA2 and EBNA-LPmediated up-regulation of S phase promoting oncoproteins including c-Myc, cyclinD2, and E2F1 ((Kaiser et al., 1999; Sinclair et al., 1994) and Fig. 6). This evidence concerns the gene TP53 and Epstein-Barr virus infection.