Infection with EV-D68 caused HuR, TiA1, and G3BP1 to colocalize, resulting in the formation of a typical SG dependent on protein kinase R (PKR) and eIF2 phosphorylation, implying that TiA1, HuR, and G3BP1 could target EV-D68's 3' untranslated region (UTR), inhibiting viral replication. This evidence concerns the gene G3BP1 and infection.