Activation of Akt and downstream inactivation of GSK3β inhibitcell death and modulate cell cycle regulation by cyclin-D1,25 implicating inactivation of GSK3β as potential requirement for theinhibition of extrinsic pathway-triggered apoptosis during early viral infection.This hypothesis is consistent with findings from the current study in which weobserved Ser9 phosphorylation and inactivation of GSK3β at early-infection timepoints. Here, AKT1 is linked to viral infectious disease.