Coronavirus infection, ER stress and Apoptosis
The replication of coronavirus, a family of important animal and human pathogens, is closely associated with the cellular membrane compartments, especially the endoplasmic reticulum (ER). Coronavirus infection of cultured cells was previously shown to cause ER stress and induce the unfolded protein...
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2014-06-01
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doaj-02402d92ba294ded9deaf664f2b7f1a22020-11-24T20:44:09ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2014-06-01510.3389/fmicb.2014.0029692793Coronavirus infection, ER stress and ApoptosisTO SING eFUNG0Ding Xiang eLiu1Nanyang Technological UniversityNanyang Technological UniversityThe replication of coronavirus, a family of important animal and human pathogens, is closely associated with the cellular membrane compartments, especially the endoplasmic reticulum (ER). Coronavirus infection of cultured cells was previously shown to cause ER stress and induce the unfolded protein response (UPR), a process that aims to restore the ER homeostasis by global translation shutdown and increasing the ER folding capacity. However under prolonged ER stress, UPR can also induce apoptotic cell death. Accumulating evidence from recent studies has shown that induction of ER stress and UPR may constitute a major aspect of coronavirus-host interaction. Activation of the three branches of UPR modulates a wide variety of signaling pathways, such as mitogen-activated protein (MAP) kinases activation, autophagy, apoptosis and innate immune response. ER stress and UPR activation may therefore contribute significantly to the viral replication and pathogenesis during coronavirus infection. In this review, we summarize current knowledge on coronavirus-induced ER stress and UPR activation, with emphasis on their cross-talking to apoptotic signaling.http://journal.frontiersin.org/Journal/10.3389/fmicb.2014.00296/fullApoptosisCoronavirusUnfolded Protein Responseer stresssignal transduction pathwaysproinflammatory cytokines |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
TO SING eFUNG Ding Xiang eLiu |
spellingShingle |
TO SING eFUNG Ding Xiang eLiu Coronavirus infection, ER stress and Apoptosis Frontiers in Microbiology Apoptosis Coronavirus Unfolded Protein Response er stress signal transduction pathways proinflammatory cytokines |
author_facet |
TO SING eFUNG Ding Xiang eLiu |
author_sort |
TO SING eFUNG |
title |
Coronavirus infection, ER stress and Apoptosis |
title_short |
Coronavirus infection, ER stress and Apoptosis |
title_full |
Coronavirus infection, ER stress and Apoptosis |
title_fullStr |
Coronavirus infection, ER stress and Apoptosis |
title_full_unstemmed |
Coronavirus infection, ER stress and Apoptosis |
title_sort |
coronavirus infection, er stress and apoptosis |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Microbiology |
issn |
1664-302X |
publishDate |
2014-06-01 |
description |
The replication of coronavirus, a family of important animal and human pathogens, is closely associated with the cellular membrane compartments, especially the endoplasmic reticulum (ER). Coronavirus infection of cultured cells was previously shown to cause ER stress and induce the unfolded protein response (UPR), a process that aims to restore the ER homeostasis by global translation shutdown and increasing the ER folding capacity. However under prolonged ER stress, UPR can also induce apoptotic cell death. Accumulating evidence from recent studies has shown that induction of ER stress and UPR may constitute a major aspect of coronavirus-host interaction. Activation of the three branches of UPR modulates a wide variety of signaling pathways, such as mitogen-activated protein (MAP) kinases activation, autophagy, apoptosis and innate immune response. ER stress and UPR activation may therefore contribute significantly to the viral replication and pathogenesis during coronavirus infection. In this review, we summarize current knowledge on coronavirus-induced ER stress and UPR activation, with emphasis on their cross-talking to apoptotic signaling. |
topic |
Apoptosis Coronavirus Unfolded Protein Response er stress signal transduction pathways proinflammatory cytokines |
url |
http://journal.frontiersin.org/Journal/10.3389/fmicb.2014.00296/full |
work_keys_str_mv |
AT tosingefung coronavirusinfectionerstressandapoptosis AT dingxiangeliu coronavirusinfectionerstressandapoptosis |
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1716818251849138176 |