The re-localization of ARGLU1 within the infected cells was not dependent on the ability of ARGLU1 to bind to E1A as the mutant dl1102 showed similar ARGLU1 phenotype to dl309, suggesting that it is infection or virus replication that is causing alteration in sub-nuclear ARGLU1 distribution rather than E1A binding per se. Here, DHTKD1 is linked to infection.