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Viruses 2016, 8(5), 124; doi:10.3390/v8050124

Respiratory Syncytial Virus and Cellular Stress Responses: Impact on Replication and Physiopathology

1
CRCHUM—Centre Hospitalier de l’Université de Montréal, Montréal, QC H2X 0A9, Canada
2
Faculty of Medicine, Université de Montréal, Montréal, QC H3C 3J7, Canada
3
Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montréal, QC H3C 3J7, Canada
4
Department of Biochemistry and Molecular Medicine, Université de Montréal, Montréal, QC H3C 3J7, Canada
Authors contributed equally.
*
Author to whom correspondence should be addressed.
Academic Editor: Craig McCormick
Received: 9 March 2016 / Revised: 14 April 2016 / Accepted: 21 April 2016 / Published: 12 May 2016
(This article belongs to the Special Issue Viral Subversion of Stress Responses and Translational Control)
View Full-Text   |   Download PDF [1213 KB, uploaded 12 May 2016]   |  

Abstract

Human respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, is a major cause of severe acute lower respiratory tract infection in infants, elderly and immunocompromised adults. Despite decades of research, a complete integrated picture of RSV-host interaction is still missing. Several cellular responses to stress are involved in the host-response to many virus infections. The endoplasmic reticulum stress induced by altered endoplasmic reticulum (ER) function leads to activation of the unfolded-protein response (UPR) to restore homeostasis. Formation of cytoplasmic stress granules containing translationally stalled mRNAs is a means to control protein translation. Production of reactive oxygen species is balanced by an antioxidant response to prevent oxidative stress and the resulting damages. In recent years, ongoing research has started to unveil specific regulatory interactions of RSV with these host cellular stress responses. Here, we discuss the latest findings regarding the mechanisms evolved by RSV to induce, subvert or manipulate the ER stress, the stress granule and oxidative stress responses. We summarize the evidence linking these stress responses with the regulation of RSV replication and the associated pathogenesis. View Full-Text
Keywords: virus; respiratory syncytial virus; RSV; stress response; endoplasmic reticulum; ER stress; stress granule; reactive oxygen species; oxidative stress; inclusion bodies virus; respiratory syncytial virus; RSV; stress response; endoplasmic reticulum; ER stress; stress granule; reactive oxygen species; oxidative stress; inclusion bodies
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Cervantes-Ortiz, S.L.; Zamorano Cuervo, N.; Grandvaux, N. Respiratory Syncytial Virus and Cellular Stress Responses: Impact on Replication and Physiopathology. Viruses 2016, 8, 124.

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