AKT1 and Rotavirus infection: We have previously confirmed that the PI3K-Akt-mTOR pathway sustains rotavirus infection via its downstream effector 4E-BP1 [39], which provokes us to further investigate the effect of eIF4E on rotavirus infection, since mTOR exerts the function of splitting the 4E-BP1-eIF4E dimer via phosphorylating 4E-BP1 [40].