Influenza Virus Non-Structural Protein 1 (NS1) Disrupts Interferon Signaling
Type I interferons (IFNs) function as the first line of defense against viral infections by modulating cell growth, establishing an antiviral state and influencing the activation of various immune cells. Viruses such as influenza have developed mechanisms to evade this defense mechanism and during i...
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| Published in | PloS one Vol. 5; no. 11; p. e13927 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
10.11.2010
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Type I interferons (IFNs) function as the first line of defense against viral infections by modulating cell growth, establishing an antiviral state and influencing the activation of various immune cells. Viruses such as influenza have developed mechanisms to evade this defense mechanism and during infection with influenza A viruses, the non-structural protein 1 (NS1) encoded by the virus genome suppresses induction of IFNs-α/β. Here we show that expression of avian H5N1 NS1 in HeLa cells leads to a block in IFN signaling. H5N1 NS1 reduces IFN-inducible tyrosine phosphorylation of STAT1, STAT2 and STAT3 and inhibits the nuclear translocation of phospho-STAT2 and the formation of IFN-inducible STAT1:1-, STAT1:3- and STAT3:3- DNA complexes. Inhibition of IFN-inducible STAT signaling by NS1 in HeLa cells is, in part, a consequence of NS1-mediated inhibition of expression of the IFN receptor subunit, IFNAR1. In support of this NS1-mediated inhibition, we observed a reduction in expression of ifnar1 in ex vivo human non-tumor lung tissues infected with H5N1 and H1N1 viruses. Moreover, H1N1 and H5N1 virus infection of human monocyte-derived macrophages led to inhibition of both ifnar1 and ifnar2 expression. In addition, NS1 expression induces up-regulation of the JAK/STAT inhibitors, SOCS1 and SOCS3. By contrast, treatment of ex vivo human lung tissues with IFN-α results in the up-regulation of a number of IFN-stimulated genes and inhibits both H5N1 and H1N1 virus replication. The data suggest that NS1 can directly interfere with IFN signaling to enhance viral replication, but that treatment with IFN can nevertheless override these inhibitory effects to block H5N1 and H1N1 virus infections. |
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| AbstractList | Type I interferons (IFNs) function as the first line of defense against viral infections by modulating cell growth, establishing an antiviral state and influencing the activation of various immune cells. Viruses such as influenza have developed mechanisms to evade this defense mechanism and during infection with influenza A viruses, the non-structural protein 1 (NS1) encoded by the virus genome suppresses induction of IFNs-[alpha]/[beta]. Here we show that expression of avian H5N1 NS1 in HeLa cells leads to a block in IFN signaling. H5N1 NS1 reduces IFN-inducible tyrosine phosphorylation of STAT1, STAT2 and STAT3 and inhibits the nuclear translocation of phospho-STAT2 and the formation of IFN-inducible STAT1:1-, STAT1:3- and STAT3:3- DNA complexes. Inhibition of IFN-inducible STAT signaling by NS1 in HeLa cells is, in part, a consequence of NS1-mediated inhibition of expression of the IFN receptor subunit, IFNAR1. In support of this NS1-mediated inhibition, we observed a reduction in expression of ifnar1 in ex vivo human non-tumor lung tissues infected with H5N1 and H1N1 viruses. Moreover, H1N1 and H5N1 virus infection of human monocyte-derived macrophages led to inhibition of both ifnar1 and ifnar2 expression. In addition, NS1 expression induces up-regulation of the JAK/STAT inhibitors, SOCS1 and SOCS3. By contrast, treatment of ex vivo human lung tissues with IFN-[alpha] results in the up-regulation of a number of IFN-stimulated genes and inhibits both H5N1 and H1N1 virus replication. The data suggest that NS1 can directly interfere with IFN signaling to enhance viral replication, but that treatment with IFN can nevertheless override these inhibitory effects to block H5N1 and H1N1 virus infections. Type I interferons (IFNs) function as the first line of defense against viral infections by modulating cell growth, establishing an antiviral state and influencing the activation of various immune cells. Viruses such as influenza have developed mechanisms to evade this defense mechanism and during infection with influenza A viruses, the non-structural protein 1 (NS1) encoded by the virus genome suppresses induction of IFNs-α/β. Here we show that expression of avian H5N1 NS1 in HeLa cells leads to a block in IFN signaling. H5N1 NS1 reduces IFN-inducible tyrosine phosphorylation of STAT1, STAT2 and STAT3 and inhibits the nuclear translocation of phospho-STAT2 and the formation of IFN-inducible STAT1:1-, STAT1:3- and STAT3:3- DNA complexes. Inhibition of IFN-inducible STAT signaling by NS1 in HeLa cells is, in part, a consequence of NS1-mediated inhibition of expression of the IFN receptor subunit, IFNAR1. In support of this NS1-mediated inhibition, we observed a reduction in expression of ifnar1 in ex vivo human non-tumor lung tissues infected with H5N1 and H1N1 viruses. Moreover, H1N1 and H5N1 virus infection of human monocyte-derived macrophages led to inhibition of both ifnar1 and ifnar2 expression. In addition, NS1 expression induces up-regulation of the JAK/STAT inhibitors, SOCS1 and SOCS3. By contrast, treatment of ex vivo human lung tissues with IFN-α results in the up-regulation of a number of IFN-stimulated genes and inhibits both H5N1 and H1N1 virus replication. The data suggest that NS1 can directly interfere with IFN signaling to enhance viral replication, but that treatment with IFN can nevertheless override these inhibitory effects to block H5N1 and H1N1 virus infections. Type I interferons (IFNs) function as the first line of defense against viral infections by modulating cell growth, establishing an antiviral state and influencing the activation of various immune cells. Viruses such as influenza have developed mechanisms to evade this defense mechanism and during infection with influenza A viruses, the non-structural protein 1 (NS1) encoded by the virus genome suppresses induction of IFNs-α/β. Here we show that expression of avian H5N1 NS1 in HeLa cells leads to a block in IFN signaling. H5N1 NS1 reduces IFN-inducible tyrosine phosphorylation of STAT1, STAT2 and STAT3 and inhibits the nuclear translocation of phospho-STAT2 and the formation of IFN-inducible STAT1:1-, STAT1:3- and STAT3:3- DNA complexes. Inhibition of IFN-inducible STAT signaling by NS1 in HeLa cells is, in part, a consequence of NS1-mediated inhibition of expression of the IFN receptor subunit, IFNAR1. In support of this NS1-mediated inhibition, we observed a reduction in expression of ifnar1 in ex vivo human non-tumor lung tissues infected with H5N1 and H1N1 viruses. Moreover, H1N1 and H5N1 virus infection of human monocyte-derived macrophages led to inhibition of both ifnar1 and ifnar2 expression. In addition, NS1 expression induces up-regulation of the JAK/STAT inhibitors, SOCS1 and SOCS3. By contrast, treatment of ex vivo human lung tissues with IFN-α results in the up-regulation of a number of IFN-stimulated genes and inhibits both H5N1 and H1N1 virus replication. The data suggest that NS1 can directly interfere with IFN signaling to enhance viral replication, but that treatment with IFN can nevertheless override these inhibitory effects to block H5N1 and H1N1 virus infections. Type I interferons (IFNs) function as the first line of defense against viral infections by modulating cell growth, establishing an antiviral state and influencing the activation of various immune cells. Viruses such as influenza have developed mechanisms to evade this defense mechanism and during infection with influenza A viruses, the non-structural protein 1 (NS1) encoded by the virus genome suppresses induction of IFNs-α/β. Here we show that expression of avian H5N1 NS1 in HeLa cells leads to a block in IFN signaling. H5N1 NS1 reduces IFN-inducible tyrosine phosphorylation of STAT1, STAT2 and STAT3 and inhibits the nuclear translocation of phospho-STAT2 and the formation of IFN-inducible STAT1:1-, STAT1:3- and STAT3:3- DNA complexes. Inhibition of IFN-inducible STAT signaling by NS1 in HeLa cells is, in part, a consequence of NS1-mediated inhibition of expression of the IFN receptor subunit, IFNAR1. In support of this NS1-mediated inhibition, we observed a reduction in expression of ifnar1 in ex vivo human non-tumor lung tissues infected with H5N1 and H1N1 viruses. Moreover, H1N1 and H5N1 virus infection of human monocyte-derived macrophages led to inhibition of both ifnar1 and ifnar2 expression. In addition, NS1 expression induces up-regulation of the JAK/STAT inhibitors, SOCS1 and SOCS3. By contrast, treatment of ex vivo human lung tissues with IFN-α results in the up-regulation of a number of IFN-stimulated genes and inhibits both H5N1 and H1N1 virus replication. The data suggest that NS1 can directly interfere with IFN signaling to enhance viral replication, but that treatment with IFN can nevertheless override these inhibitory effects to block H5N1 and H1N1 virus infections.Type I interferons (IFNs) function as the first line of defense against viral infections by modulating cell growth, establishing an antiviral state and influencing the activation of various immune cells. Viruses such as influenza have developed mechanisms to evade this defense mechanism and during infection with influenza A viruses, the non-structural protein 1 (NS1) encoded by the virus genome suppresses induction of IFNs-α/β. Here we show that expression of avian H5N1 NS1 in HeLa cells leads to a block in IFN signaling. H5N1 NS1 reduces IFN-inducible tyrosine phosphorylation of STAT1, STAT2 and STAT3 and inhibits the nuclear translocation of phospho-STAT2 and the formation of IFN-inducible STAT1:1-, STAT1:3- and STAT3:3- DNA complexes. Inhibition of IFN-inducible STAT signaling by NS1 in HeLa cells is, in part, a consequence of NS1-mediated inhibition of expression of the IFN receptor subunit, IFNAR1. In support of this NS1-mediated inhibition, we observed a reduction in expression of ifnar1 in ex vivo human non-tumor lung tissues infected with H5N1 and H1N1 viruses. Moreover, H1N1 and H5N1 virus infection of human monocyte-derived macrophages led to inhibition of both ifnar1 and ifnar2 expression. In addition, NS1 expression induces up-regulation of the JAK/STAT inhibitors, SOCS1 and SOCS3. By contrast, treatment of ex vivo human lung tissues with IFN-α results in the up-regulation of a number of IFN-stimulated genes and inhibits both H5N1 and H1N1 virus replication. The data suggest that NS1 can directly interfere with IFN signaling to enhance viral replication, but that treatment with IFN can nevertheless override these inhibitory effects to block H5N1 and H1N1 virus infections. |
| Audience | Academic |
| Author | Lee, Suki M. Y. Baker, Darren P. Fish, Eleanor N. Chan, Michael C. W. Chan, Renee W. Y. Peiris, J. S. Malik Wang, Ben Xuhao Jia, Danlin Rahbar, Ramtin Sun, Bing Nicholls, John M. |
| AuthorAffiliation | 1 Department of Immunology, University of Toronto, Toronto, Canada 3 Department of Microbiology, University of Hong Kong, Hong Kong, People's Republic of China 5 Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China 2 Department of Pathology, University of Hong Kong, Hong Kong, People's Republic of China Tsinghua University, China 6 Division of Cell and Molecular Biology, Toronto General Research Institute, University Health Network, Toronto, Canada 4 Biogen Idec Inc., Cambridge, Massachusetts, United States of America |
| AuthorAffiliation_xml | – name: 1 Department of Immunology, University of Toronto, Toronto, Canada – name: 3 Department of Microbiology, University of Hong Kong, Hong Kong, People's Republic of China – name: 6 Division of Cell and Molecular Biology, Toronto General Research Institute, University Health Network, Toronto, Canada – name: Tsinghua University, China – name: 5 Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China – name: 2 Department of Pathology, University of Hong Kong, Hong Kong, People's Republic of China – name: 4 Biogen Idec Inc., Cambridge, Massachusetts, United States of America |
| Author_xml | – sequence: 1 givenname: Danlin surname: Jia fullname: Jia, Danlin – sequence: 2 givenname: Ramtin surname: Rahbar fullname: Rahbar, Ramtin – sequence: 3 givenname: Renee W. Y. surname: Chan fullname: Chan, Renee W. Y. – sequence: 4 givenname: Suki M. Y. surname: Lee fullname: Lee, Suki M. Y. – sequence: 5 givenname: Michael C. W. surname: Chan fullname: Chan, Michael C. W. – sequence: 6 givenname: Ben Xuhao surname: Wang fullname: Wang, Ben Xuhao – sequence: 7 givenname: Darren P. surname: Baker fullname: Baker, Darren P. – sequence: 8 givenname: Bing surname: Sun fullname: Sun, Bing – sequence: 9 givenname: J. S. Malik surname: Peiris fullname: Peiris, J. S. Malik – sequence: 10 givenname: John M. surname: Nicholls fullname: Nicholls, John M. – sequence: 11 givenname: Eleanor N. surname: Fish fullname: Fish, Eleanor N. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21085662$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2010 Public Library of Science 2010 Jia et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Jia et al. 2010 |
| Copyright_xml | – notice: COPYRIGHT 2010 Public Library of Science – notice: 2010 Jia et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: Jia et al. 2010 |
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| DOI | 10.1371/journal.pone.0013927 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 Conceived and designed the experiments: DJ JSMP JMN ENF. Performed the experiments: DJ RR RWYC SML MCC. Analyzed the data: DJ RR RWYC MCC BXW JSMP JMN ENF. Contributed reagents/materials/analysis tools: DPB BS JMN. Wrote the paper: DJ RR ENF. Involved in editing the manuscript and reviewing the different drafts: DPB. Provided input for data interpretation: DPB. Involved in reviewing the manuscript: BS. |
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| SubjectTerms | Antiviral state Avian influenza Avian influenza viruses Biological response modifiers Cells, Cultured Deoxyribonucleic acid Development and progression DNA Drug resistance Gene expression Gene Expression - drug effects Genes Genomes Green Fluorescent Proteins - genetics Green Fluorescent Proteins - metabolism Health aspects HeLa Cells Host-Pathogen Interactions Humans Immune system Immunoblotting Infection Infections Infectious Diseases/Viral Infections Influenza Influenza A Influenza A virus - genetics Influenza A virus - metabolism Influenza A virus - physiology Influenza A Virus, H1N1 Subtype - metabolism Influenza A Virus, H1N1 Subtype - physiology Influenza A Virus, H5N1 Subtype - metabolism Influenza A Virus, H5N1 Subtype - physiology Influenza virus Inhibition Interferon Interferons - metabolism Interferons - pharmacology Kinases Lung - drug effects Lung - metabolism Lung - virology Lungs Macrophages Macrophages - cytology Macrophages - metabolism Macrophages - virology Microscopy, Confocal Monocytes Nuclear transport Phosphorylation Receptor, Interferon alpha-beta - genetics Receptor, Interferon alpha-beta - metabolism Replication Reverse Transcriptase Polymerase Chain Reaction Signal Transduction - physiology Signaling Stat1 protein STAT1 Transcription Factor - metabolism Stat2 protein STAT2 Transcription Factor - metabolism Stat3 protein Suppressor of Cytokine Signaling 1 Protein Suppressor of Cytokine Signaling Proteins - genetics Suppressor of Cytokine Signaling Proteins - metabolism Swine flu Tissue Culture Techniques Tissues Translocation Tyrosine Viral Nonstructural Proteins - genetics Viral Nonstructural Proteins - metabolism Viral Nonstructural Proteins - physiology Virology Virology/Immune Evasion Viruses |
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| Title | Influenza Virus Non-Structural Protein 1 (NS1) Disrupts Interferon Signaling |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/21085662 https://www.proquest.com/docview/1295222429 https://www.proquest.com/docview/808461522 https://www.proquest.com/docview/874179023 https://pubmed.ncbi.nlm.nih.gov/PMC2978095 https://doaj.org/article/8c0f5d8c214f42d38650d89baf78a12d http://dx.doi.org/10.1371/journal.pone.0013927 |
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