Calicivirus infection leads to a shut-off of cellular translation and to multiple changes to the cellular translation apparatus, including phosphorylation of eIF2α, viral protease-mediated cleavage of the poly(A)-binding protein PABP, eIF4E phosphorylation, induced caspase-mediated cleavage of eIF4G and translocation of PTB from the nucleus to the cytoplasm (47,94–96). Here, EIF2A is linked to Caliciviridae infectious disease.