HCMV is a globally important opportunistic pathogen that causes severe diseases in immunocompromised individuals and is the leading viral cause of congenital diseases. This virus stimulates cell cycle progression of quiescent cells into an S phase-like environment but concurrently blocks host DNA synthesis [25] . HCMV promotes cell cycle progression likely in part by inactivating Rb [6, 26] and regulating the APC [24, 27, 28] . It has been reported that HCMV has two means to regulate the APC. The multifunctional viral kinase pUL97 phosphorylates the APC coactivator Cdh1, thus likely inhibiting its activity [24] . Nonetheless, abrogation of UL97 alone only results in a modest increase in APC activity during infection [24] . Independent of UL97mediated Cdh1 regulation, HCMV also induces degradation of two APC subunits, APC4 and APC5, leading to the dissociation of the complex during infection [24] . The viral factor and associated mechanism responsible for regulating degradation of the APC subunits have not been identified.