Interestingly, in a cell culture model of quiescent HSV-1 infection, superinfection by an ICP0 RING finger mutant virus, which was incapable of degrading PML and Sp100 and therefore incapable of dispersing ND10, did not remove heterochromatin markers from the quiescent HSV-1 genome, whereas the wild type counterpart reduced the heterochromatin markers on HSV-1 genome and reactivated the quiescent genome into productive infection [24]. This evidence concerns the gene PML and infection.