ATF6 and infection: Due to the inability of the cytoplasm to glycosylate proteins, these can only be formed as such in the endoplasmic reticulum, so the virus is bound to replicate through this organelle, making it necessary to develop defence strategies against UPR.As a result, HSV-1 replication prevents ATF6 cleavage activation, as previously described in the early stages of infection [32], and melatonin is able to reverse this blockade.