Flux of viral glycoproteins through the secretory pathway is a major contributor towards ER stress during infection . BiP binds strongly with many surface glycoproteins of respiratory viruses that are often overexpressed and misfolded during infection . As a key feature of these proteins, glycosylation, and variations in glycosylation site occupancies that may arise due to mutation, are important determinants of the folding efficiency of viral glycoproteins, and hence of UPR activation.