Mouse hepatitis coronavirus replication induces host translational shutoff and mRNA decay, with concomitant formation of stress granules and processing bodies

Summary Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed genome‐wide microarray analyses of the expression patterns of mouse hepatitis coronavirus (MHV)‐infected cells. At the time of MHV‐indu...

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Vydané v:	Cellular microbiology Ročník 9; číslo 9; s. 2218 - 2229
Hlavní autori:	Raaben, Matthijs, Groot Koerkamp, Marian J. A., Rottier, Peter J. M., De Haan, Cornelis A. M.
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Oxford, UK Blackwell Publishing Ltd 01.09.2007 John Wiley & Sons, Inc
Predmet:	Animals Cells, Cultured Coronavirus Coronavirus Infections - metabolism COVID-19 Cytoplasmic Granules - metabolism Decay Eukaryotic Initiation Factor-2 - metabolism Fibroblasts - cytology Fibroblasts - metabolism Fibroblasts - virology Hepatitis Hepatitis, Viral, Animal - metabolism Humans Mice Molecular Sequence Data Murine hepatitis virus - genetics Murine hepatitis virus - physiology Oligonucleotide Array Sequence Analysis Original Protein Biosynthesis Protein synthesis RNA Stability RNA, Messenger - metabolism Transcription, Genetic Virus Replication
ISSN:	1462-5814, 1462-5822
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Abstract	Summary Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed genome‐wide microarray analyses of the expression patterns of mouse hepatitis coronavirus (MHV)‐infected cells. At the time of MHV‐induced host translational shutoff, downregulation of numerous mRNAs, many of which encode protein translation‐related factors, was observed. This downregulation, which is reminiscent of a cellular stress response, was dependent on viral replication and caused by mRNA decay. Concomitantly, phosphorylation of the eukaryotic translation initiation factor 2α was increased in MHV‐infected cells. In addition, stress granules and processing bodies appeared, which are sites for mRNA stalling and degradation respectively. We propose that MHV replication induces host translational shutoff by triggering an integrated stress response. However, MHV replication per se does not appear to benefit from the inhibition of host protein synthesis, at least in vitro, since viral replication was not negatively affected but rather enhanced in cells with impaired translational shutoff.
AbstractList	Summary Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed genome‐wide microarray analyses of the expression patterns of mouse hepatitis coronavirus (MHV)‐infected cells. At the time of MHV‐induced host translational shutoff, downregulation of numerous mRNAs, many of which encode protein translation‐related factors, was observed. This downregulation, which is reminiscent of a cellular stress response, was dependent on viral replication and caused by mRNA decay. Concomitantly, phosphorylation of the eukaryotic translation initiation factor 2α was increased in MHV‐infected cells. In addition, stress granules and processing bodies appeared, which are sites for mRNA stalling and degradation respectively. We propose that MHV replication induces host translational shutoff by triggering an integrated stress response. However, MHV replication per se does not appear to benefit from the inhibition of host protein synthesis, at least in vitro, since viral replication was not negatively affected but rather enhanced in cells with impaired translational shutoff. Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed genome-wide microarray analyses of the expression patterns of mouse hepatitis coronavirus (MHV)-infected cells. At the time of MHV-induced host translational shutoff, downregulation of numerous mRNAs, many of which encode protein translation-related factors, was observed. This downregulation, which is reminiscent of a cellular stress response, was dependent on viral replication and caused by mRNA decay. Concomitantly, phosphorylation of the eukaryotic translation initiation factor 2α was increased in MHV-infected cells. In addition, stress granules and processing bodies appeared, which are sites for mRNA stalling and degradation respectively. We propose that MHV replication induces host translational shutoff by triggering an integrated stress response. However, MHV replication per se does not appear to benefit from the inhibition of host protein synthesis, at least in vitro , since viral replication was not negatively affected but rather enhanced in cells with impaired translational shutoff. Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed genome-wide microarray analyses of the expression patterns of mouse hepatitis coronavirus (MHV)-infected cells. At the time of MHV-induced host translational shutoff, downregulation of numerous mRNAs, many of which encode protein translation-related factors, was observed. This downregulation, which is reminiscent of a cellular stress response, was dependent on viral replication and caused by mRNA decay. Concomitantly, phosphorylation of the eukaryotic translation initiation factor 2alpha was increased in MHV-infected cells. In addition, stress granules and processing bodies appeared, which are sites for mRNA stalling and degradation respectively. We propose that MHV replication induces host translational shutoff by triggering an integrated stress response. However, MHV replication per se does not appear to benefit from the inhibition of host protein synthesis, at least in vitro, since viral replication was not negatively affected but rather enhanced in cells with impaired translational shutoff. Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed genome-wide microarray analyses of the expression patterns of mouse hepatitis coronavirus (MHV)-infected cells. At the time of MHV-induced host translational shutoff, downregulation of numerous mRNAs, many of which encode protein translation-related factors, was observed. This downregulation, which is reminiscent of a cellular stress response, was dependent on viral replication and caused by mRNA decay. Concomitantly, phosphorylation of the eukaryotic translation initiation factor 2alpha was increased in MHV-infected cells. In addition, stress granules and processing bodies appeared, which are sites for mRNA stalling and degradation respectively. We propose that MHV replication induces host translational shutoff by triggering an integrated stress response. However, MHV replication per se does not appear to benefit from the inhibition of host protein synthesis, at least in vitro, since viral replication was not negatively affected but rather enhanced in cells with impaired translational shutoff.Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed genome-wide microarray analyses of the expression patterns of mouse hepatitis coronavirus (MHV)-infected cells. At the time of MHV-induced host translational shutoff, downregulation of numerous mRNAs, many of which encode protein translation-related factors, was observed. This downregulation, which is reminiscent of a cellular stress response, was dependent on viral replication and caused by mRNA decay. Concomitantly, phosphorylation of the eukaryotic translation initiation factor 2alpha was increased in MHV-infected cells. In addition, stress granules and processing bodies appeared, which are sites for mRNA stalling and degradation respectively. We propose that MHV replication induces host translational shutoff by triggering an integrated stress response. However, MHV replication per se does not appear to benefit from the inhibition of host protein synthesis, at least in vitro, since viral replication was not negatively affected but rather enhanced in cells with impaired translational shutoff. Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed genome-wide microarray analyses of the expression patterns of mouse hepatitis coronavirus (MHV)-infected cells. At the time of MHV-induced host translational shutoff, downregulation of numerous mRNAs, many of which encode protein translation-related factors, was observed. This downregulation, which is reminiscent of a cellular stress response, was dependent on viral replication and caused by mRNA decay. Concomitantly, phosphorylation of the eukaryotic translation initiation factor 2 alpha was increased in MHV-infected cells. In addition, stress granules and processing bodies appeared, which are sites for mRNA stalling and degradation respectively. We propose that MHV replication induces host translational shutoff by triggering an integrated stress response. However, MHV replication per se does not appear to benefit from the inhibition of host protein synthesis, at least in vitro, since viral replication was not negatively affected but rather enhanced in cells with impaired translational shutoff.
Author	Raaben, Matthijs Groot Koerkamp, Marian J. A. De Haan, Cornelis A. M. Rottier, Peter J. M.
AuthorAffiliation	1 Virology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, the Netherlands 2 Microarray Facility, UMC Utrecht, Department of Physiological Chemistry, Utrecht, the Netherlands
AuthorAffiliation_xml	– name: 2 Microarray Facility, UMC Utrecht, Department of Physiological Chemistry, Utrecht, the Netherlands – name: 1 Virology Division, Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, the Netherlands
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/17490409$$D View this record in MEDLINE/PubMed
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Snippet	Summary Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we... Many viruses, including coronaviruses, induce host translational shutoff, while maintaining synthesis of their own gene products. In this study we performed...
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SubjectTerms	Animals Cells, Cultured Coronavirus Coronavirus Infections - metabolism COVID-19 Cytoplasmic Granules - metabolism Decay Eukaryotic Initiation Factor-2 - metabolism Fibroblasts - cytology Fibroblasts - metabolism Fibroblasts - virology Hepatitis Hepatitis, Viral, Animal - metabolism Humans Mice Molecular Sequence Data Murine hepatitis virus - genetics Murine hepatitis virus - physiology Oligonucleotide Array Sequence Analysis Original Protein Biosynthesis Protein synthesis RNA Stability RNA, Messenger - metabolism Transcription, Genetic Virus Replication
Title	Mouse hepatitis coronavirus replication induces host translational shutoff and mRNA decay, with concomitant formation of stress granules and processing bodies
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