The paradigm in virus infection is that levels of virus replication should be inversely correlated with levels of apoptosis, as we previously observed in Bcl-2 overexpressing U937 cells infected with HSV-232 and in a less pronounced manner with HSV-1.31 Given that disruption of NF-κB activation enhanced HSV-1 replication in monocytic cells we could expect that levels of apoptosis should be concomitantly diminished. Here, BCL2 is linked to viral infectious disease.