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Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis
During viral infection, the host cell synthesizes high amounts of viral proteins, which often causes stress to the endoplasmic reticulum (ER). To manage abnormal ER stress, mammalian cells trigger a response called the unfolded protein response (UPR). Previous studies have indicated that porcine rep...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7403369/ https://www.ncbi.nlm.nih.gov/pubmed/32753633 http://dx.doi.org/10.1038/s41598-020-69959-z |
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author | Chen, Quangang Men, Yanjuan Wang, Dang Xu, Deqin Liu, Suyan Xiao, Shaobo Fang, Liurong |
author_facet | Chen, Quangang Men, Yanjuan Wang, Dang Xu, Deqin Liu, Suyan Xiao, Shaobo Fang, Liurong |
author_sort | Chen, Quangang |
collection | PubMed |
description | During viral infection, the host cell synthesizes high amounts of viral proteins, which often causes stress to the endoplasmic reticulum (ER). To manage abnormal ER stress, mammalian cells trigger a response called the unfolded protein response (UPR). Previous studies have indicated that porcine reproductive and respiratory syndrome virus (PRRSV), an Arterivirus that has been devastating the swine industry worldwide, can induce ER stress and activate UPR, however, the activation pathways and the biological significance requires further investigation. In this study, we demonstrated that, among the three types of UPR pathways, PRRSV infection induced PERK and IRE1 pathways, but not the ATF6 pathway. Furthermore, the induction of UPR promoted PRRSV replication. We also found that PRRSV-induced UPR, particularly the PERK pathway, was involved in the induction of autophagy, a cellular degradation process that can alleviate cell stress. Besides, we also provided insights into the ER stress-mediated apoptosis in response to PRRSV infection. PRRSV infection induced the expression of the transcription factor CHOP, which activated caspase 3 and PARP led to ER stress-mediated apoptosis. Using 3-Methyladenine (3-MA) to inhibit autophagy, the increased ER stress and cell apoptosis were observed in the PRRSV infected cell. Taken together, our results revealed the associations of ER stress, autophagy, and apoptosis during PRRSV infection, helping us to further understand how PRRSV interacts with host cells. |
format | Online Article Text |
id | pubmed-7403369 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-74033692020-08-07 Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis Chen, Quangang Men, Yanjuan Wang, Dang Xu, Deqin Liu, Suyan Xiao, Shaobo Fang, Liurong Sci Rep Article During viral infection, the host cell synthesizes high amounts of viral proteins, which often causes stress to the endoplasmic reticulum (ER). To manage abnormal ER stress, mammalian cells trigger a response called the unfolded protein response (UPR). Previous studies have indicated that porcine reproductive and respiratory syndrome virus (PRRSV), an Arterivirus that has been devastating the swine industry worldwide, can induce ER stress and activate UPR, however, the activation pathways and the biological significance requires further investigation. In this study, we demonstrated that, among the three types of UPR pathways, PRRSV infection induced PERK and IRE1 pathways, but not the ATF6 pathway. Furthermore, the induction of UPR promoted PRRSV replication. We also found that PRRSV-induced UPR, particularly the PERK pathway, was involved in the induction of autophagy, a cellular degradation process that can alleviate cell stress. Besides, we also provided insights into the ER stress-mediated apoptosis in response to PRRSV infection. PRRSV infection induced the expression of the transcription factor CHOP, which activated caspase 3 and PARP led to ER stress-mediated apoptosis. Using 3-Methyladenine (3-MA) to inhibit autophagy, the increased ER stress and cell apoptosis were observed in the PRRSV infected cell. Taken together, our results revealed the associations of ER stress, autophagy, and apoptosis during PRRSV infection, helping us to further understand how PRRSV interacts with host cells. Nature Publishing Group UK 2020-08-04 /pmc/articles/PMC7403369/ /pubmed/32753633 http://dx.doi.org/10.1038/s41598-020-69959-z Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Chen, Quangang Men, Yanjuan Wang, Dang Xu, Deqin Liu, Suyan Xiao, Shaobo Fang, Liurong Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis |
title | Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis |
title_full | Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis |
title_fullStr | Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis |
title_full_unstemmed | Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis |
title_short | Porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis |
title_sort | porcine reproductive and respiratory syndrome virus infection induces endoplasmic reticulum stress, facilitates virus replication, and contributes to autophagy and apoptosis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7403369/ https://www.ncbi.nlm.nih.gov/pubmed/32753633 http://dx.doi.org/10.1038/s41598-020-69959-z |
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