To verify if activation of the ATR/Chk1 pathway is dependent from productive EBV infection or rather form EBV or cellular components that might have co-purified with the virus, we monitored ATR, Chk1, ATM and Chk2 following inoculation of purified CD19+ TBCs with EBV-B95.8 or UV-inactivated EBV-B95.8. The gene discussed is ATR; the disease is Epstein-Barr virus infection.