Several viral factors from different viral families have been reported to use diverse mechanisms to regulate the APC. For instance, the human papillomavirus E2 protein binds to and inhibits the Cdh1 activator protein [20] , while the parapoxvirus virus protein PACR (poxviral APC regulator) functions as an enzymatically inactive APC11 mimic [23, 37] . The chicken anemia virus (CAV) protein apoptin can bind to the APC at the bridge and cause its dissociation using an unknown mechanism [19] . The fact that proteins from both HCMV and CAV target the APC bridge subcomplex suggests that viruses have evolved regulatory strategies converging on this sub-complex as an efficient means to disable APC activity. It is intriguing to speculate that modulating the APC complex by dissolving the bridge may allow viruses to alter substrate specificity of the APC instead of completely abolishing its activity, as the enzymatic portion of APC is known to have activity in vitro [23, 38] . HCMV does not appear to directly destroy the enzymatic subcomplex of APC, so it is of interest to determine if the APC retains some activity or is directed to target different substrates during virus infection.