In general, viral favors the activation of ATF6 and IRE1 pathways as the prosurvival downstream effectors of those signaling; however, in our case, we found that the ATF6 signaling is slightly repressed in at the mid stages of infection, we think that maybe the up-regulation of GRP78 mediated by IRE1 pathway at the early stages of infection that inhibit ATF6 migrates to the Golgi apparatus. The gene discussed is HSPA5; the disease is infection.