Though relevant examples are lacking in regulation of UPR, previous work on human cytomegalovirus (beta-herpesvirus) has shown that viral infection can upregulate GRP78 expression without affecting the UPR pathways55, while studies on the herpes simplex virus type 2 (alpha-herpesvirus) revealed that the virus can encode a protein with chaperone-like activity. This evidence concerns the gene HSPA5 and viral infectious disease.