In contrast to the tunicamycin (Tm) control and live ZIKV infection and similar to the mock-infected control, UV-inactivated ZIKV did not induce phosphorylation of PERK, eIF2α, and IRE1α, ATF6 cleavage, XBP1 splicing, or ATF4 and CHOP expression at 24 and 48 hpi, confirming that UPR activation requires active ZIKV infection and replication (Fig. 4b). This evidence concerns the gene DDIT3 and Zika virus infectious disease.