Many reports have demonstrated that the kinetics of protein synthesis shutoff and eIF4GI cleavage are not correlated in PV-infected cells [120] [121] [122] . These data clearly indicate that additional translation factors may be cleaved to achieve an efficient inhibition of cellular mRNA translation. In this regard, additional reports showed that eIF4GII is also proteolyzed by 2A pro during PV and HRV infections and that this cleavage is exerted between amino acids 699/700 leading to a proteolytic pattern similar to eIF4GI. Interestingly, eIF4GII is significantly more resistant to 2A pro -mediated cleavage than eIF4GI and the kinetics of protein synthesis shutoff close correlates with eIF4GII cleavage in PV-and RHV-infected cells [122, 123] . In those studies, Gradi and colleagues proposed that hydrolysis of both eIF4GI and eIF4GII is required for achieving PV-and HRV-mediated inhibition of host-cell mRNA translation and that the cleavage of eIF4GII is the rate-limiting step in the shutoff of host-cell translation after infection with those viruses [122, 123] .