TP53 and infection: A theoretical explanation may be that the disruption of the UL39 gene (as a viral anti-apoptotic factor) [19] and p53 overexpression during replication of ΔUL39/Δγ34.5/HSV-p53 activate both intrinsic and extrinsic pathways of apoptosis in the virus- infected cancer cells accelerating the premature death, thereby limiting the virus replication to an abortive infection in cells.