Cargando…
Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling
Viruses must hijack cellular translation machinery to express viral genes. In many cases, this is impeded by cellular stress responses. These stress responses result in the global inhibition of translation and the storage of stalled mRNAs, into RNA-protein aggregates called stress granules. This res...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7291021/ https://www.ncbi.nlm.nih.gov/pubmed/32422883 http://dx.doi.org/10.3390/v12050536 |
_version_ | 1783545812804960256 |
---|---|
author | Brownsword, Matthew J. Doyle, Nicole Brocard, Michèle Locker, Nicolas Maier, Helena J. |
author_facet | Brownsword, Matthew J. Doyle, Nicole Brocard, Michèle Locker, Nicolas Maier, Helena J. |
author_sort | Brownsword, Matthew J. |
collection | PubMed |
description | Viruses must hijack cellular translation machinery to express viral genes. In many cases, this is impeded by cellular stress responses. These stress responses result in the global inhibition of translation and the storage of stalled mRNAs, into RNA-protein aggregates called stress granules. This results in the translational silencing of the majority of mRNAs excluding those beneficial for the cell to resolve the specific stress. For example, the expression of antiviral factors is maintained during viral infection. Here we investigated stress granule regulation by Gammacoronavirus infectious bronchitis virus (IBV), which causes the economically important poultry disease, infectious bronchitis. Interestingly, we found that IBV is able to inhibit multiple cellular stress granule signaling pathways, whilst at the same time, IBV replication also results in the induction of seemingly canonical stress granules in a proportion of infected cells. Moreover, IBV infection uncouples translational repression and stress granule formation and both processes are independent of eIF2α phosphorylation. These results provide novel insights into how IBV modulates cellular translation and antiviral stress signaling. |
format | Online Article Text |
id | pubmed-7291021 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-72910212020-06-17 Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling Brownsword, Matthew J. Doyle, Nicole Brocard, Michèle Locker, Nicolas Maier, Helena J. Viruses Article Viruses must hijack cellular translation machinery to express viral genes. In many cases, this is impeded by cellular stress responses. These stress responses result in the global inhibition of translation and the storage of stalled mRNAs, into RNA-protein aggregates called stress granules. This results in the translational silencing of the majority of mRNAs excluding those beneficial for the cell to resolve the specific stress. For example, the expression of antiviral factors is maintained during viral infection. Here we investigated stress granule regulation by Gammacoronavirus infectious bronchitis virus (IBV), which causes the economically important poultry disease, infectious bronchitis. Interestingly, we found that IBV is able to inhibit multiple cellular stress granule signaling pathways, whilst at the same time, IBV replication also results in the induction of seemingly canonical stress granules in a proportion of infected cells. Moreover, IBV infection uncouples translational repression and stress granule formation and both processes are independent of eIF2α phosphorylation. These results provide novel insights into how IBV modulates cellular translation and antiviral stress signaling. MDPI 2020-05-14 /pmc/articles/PMC7291021/ /pubmed/32422883 http://dx.doi.org/10.3390/v12050536 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Brownsword, Matthew J. Doyle, Nicole Brocard, Michèle Locker, Nicolas Maier, Helena J. Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling |
title | Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling |
title_full | Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling |
title_fullStr | Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling |
title_full_unstemmed | Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling |
title_short | Infectious Bronchitis Virus Regulates Cellular Stress Granule Signaling |
title_sort | infectious bronchitis virus regulates cellular stress granule signaling |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7291021/ https://www.ncbi.nlm.nih.gov/pubmed/32422883 http://dx.doi.org/10.3390/v12050536 |
work_keys_str_mv | AT brownswordmatthewj infectiousbronchitisvirusregulatescellularstressgranulesignaling AT doylenicole infectiousbronchitisvirusregulatescellularstressgranulesignaling AT brocardmichele infectiousbronchitisvirusregulatescellularstressgranulesignaling AT lockernicolas infectiousbronchitisvirusregulatescellularstressgranulesignaling AT maierhelenaj infectiousbronchitisvirusregulatescellularstressgranulesignaling |