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Many viruses (HSV1, polyomavirus, HIV1) require the activation ofATM (+/-Mre1 1) for a fully permissive infection.However, the extended life cycle of HCMV may require specialized interactions with the DNA repair machinery to maximize its ability to replicate.We have undertaken a thorough investigation of the response of permissive fibroblasts to HCMV infection.No dramatic immediate damage response to the double-stranded ends of the linear incoming virus is observed in fibroblasts.However, a constant low level ofphosphorylated ATM is apparently enough to signal its downstream targets, p53 and Nbs1.