How does the stressed out ER find relief during virus infection?

Abstract

The endoplasmic reticulum and Golgi network (ERGN) is vital to most cellular biosynthetic processes. Many positive strand RNA viruses depend upon the ERGN for replication, maturation, and egress. Viruses induce changes in ER architecture and stimulate fatty acid synthesis to create environments that can scaffold replication complexes, plant virus movement complexes, or virion maturation. Potato virus X (PVX) and Turnip mosaic virus (TuMV) each encode small membrane binding proteins that embed in the ERGN and activate the unfolded protein response (UPR). The UPR ensures ERGN homeostasis in the face of environmental assaults that could negatively impact the biosynthetic functions of the ERGN. This article explores the relationship between ER stress, the UPR, and membrane synthesis occurring during virus infection.