Thus, in stark contrast to its anti-viral function at the start of lytic infection, ATRX seems to act in a pro-viral manner at later times, perhaps explaining why HCMV (unlike HSV-1 and KSHV) does not directly target ATRX [3,46] and why its binding partner Daxx is allowed to reaccumulate after initial degradation in cells lytically infected with HCMV. This evidence concerns the gene DAXX and infection.