title: Hepatitis C virus, ER stress, and oxidative stress.
abstract: Hepatitis C virus (HCV) replication is associated with the endoplasmic reticulum (ER), where the virus causes stress. Cells cope with ER stress by activating an adaptive program called the unfolded protein response (UPR), which alleviates this stress by stimulating protein folding and degradation in the ER and down-regulating overall protein synthesis. Recent work suggests that HCV also alters ER calcium homeostasis, inducing oxidative stress. Future progress in understanding the control that HCV exerts over the ER will provide insight into viral strategies for pathogenesis and persistence in chronically infected patients.
authors.affiliation: Department of Microbiology and Program in Molecular Biology, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
authors.forename: Keith D
authors.initials: KD
authors.lastname: Tardif
authors.forename: Gulam
authors.initials: G
authors.lastname: Waris
authors.forename: Aleem
authors.initials: A
authors.lastname: Siddiqui
mesh_terms: D000222:Adaptation, Physiological; D002118:Calcium / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000502:physiology* / Q000821:virology*; D016174:Hepacivirus / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D018384:Oxidative Stress; D011506:Proteins / Q000378:metabolism
chemical_list: D011506:Proteins; D002118:Calcium