Next Article in Journal
Virus-like Particle-Based L2 Vaccines against HPVs: Where Are We Today?
Next Article in Special Issue
IRE1α Promotes Zika Virus Infection via XBP1
Previous Article in Journal
Identifying Early Warning Signals for the Sudden Transition from Mild to Severe Tobacco Etch Disease by Dynamical Network Biomarkers
Previous Article in Special Issue
The Porcine Deltacoronavirus Replication Organelle Comprises Double-Membrane Vesicles and Zippered Endoplasmic Reticulum with Double-Membrane Spherules
Open AccessReview

Herpesviruses and the Unfolded Protein Response

1
Department of Microbiology & Immunology, Dalhousie University, 5850 College Street, Halifax, NS B3H 4R2, Canada
2
Beatrice Hunter Cancer Research Institute, 5850 College Street, Halifax, NS B3H 4R2, Canada
*
Author to whom correspondence should be addressed.
Viruses 2020, 12(1), 17; https://doi.org/10.3390/v12010017
Received: 3 December 2019 / Revised: 19 December 2019 / Accepted: 19 December 2019 / Published: 21 December 2019
(This article belongs to the Special Issue Viruses and the Unfolded Protein Response)
Herpesviruses usurp cellular stress responses to promote viral replication and avoid immune surveillance. The unfolded protein response (UPR) is a conserved stress response that is activated when the protein load in the ER exceeds folding capacity and misfolded proteins accumulate. The UPR aims to restore protein homeostasis through translational and transcriptional reprogramming; if homeostasis cannot be restored, the UPR switches from “helper” to “executioner”, triggering apoptosis. It is thought that the burst of herpesvirus glycoprotein synthesis during lytic replication causes ER stress, and that these viruses may have evolved mechanisms to manage UPR signaling to create an optimal niche for replication. The past decade has seen considerable progress in understanding how herpesviruses reprogram the UPR. Here we provide an overview of the molecular events of UPR activation, signaling and transcriptional outputs, and highlight key evidence that herpesviruses hijack the UPR to aid infection. View Full-Text
Keywords: unfolded protein response (UPR); integrated stress response (ISR); ATF6; IRE1; XBP1; PERK; ATF4; GADD34; herpesvirus; Kaposi’s sarcoma-associated herpesvirus (KSHV); cytomegalovirus (CMV); herpes simplex virus (HSV) unfolded protein response (UPR); integrated stress response (ISR); ATF6; IRE1; XBP1; PERK; ATF4; GADD34; herpesvirus; Kaposi’s sarcoma-associated herpesvirus (KSHV); cytomegalovirus (CMV); herpes simplex virus (HSV)
Show Figures

Figure 1

MDPI and ACS Style

Johnston, B.P.; McCormick, C. Herpesviruses and the Unfolded Protein Response. Viruses 2020, 12, 17. https://doi.org/10.3390/v12010017

AMA Style

Johnston BP, McCormick C. Herpesviruses and the Unfolded Protein Response. Viruses. 2020; 12(1):17. https://doi.org/10.3390/v12010017

Chicago/Turabian Style

Johnston, Benjamin P.; McCormick, Craig. 2020. "Herpesviruses and the Unfolded Protein Response" Viruses 12, no. 1: 17. https://doi.org/10.3390/v12010017

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop