Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses
Summary: Type I interferons (IFNs) are our first line of defense against virus infection. Recent studies have suggested the ability of SARS-CoV-2 proteins to inhibit IFN responses. Emerging data also suggest that timing and extent of IFN production is associated with manifestation of COVID-19 severi...
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| Format: | Article |
| Language: | English |
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Elsevier
2021-05-01
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| Series: | iScience |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2589004221004454 |
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doaj-7903286efe6640018b5c5ad804e712c6 |
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| record_format |
Article |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Arinjay Banerjee Nader El-Sayes Patrick Budylowski Rajesh Abraham Jacob Daniel Richard Hassaan Maan Jennifer A. Aguiar Wael L. Demian Kaushal Baid Michael R. D'Agostino Jann Catherine Ang Tetyana Murdza Benjamin J.-M. Tremblay Sam Afkhami Mehran Karimzadeh Aaron T. Irving Lily Yip Mario Ostrowski Jeremy A. Hirota Robert Kozak Terence D. Capellini Matthew S. Miller Bo Wang Samira Mubareka Allison J. McGeer Andrew G. McArthur Andrew C. Doxey Karen Mossman |
| spellingShingle |
Arinjay Banerjee Nader El-Sayes Patrick Budylowski Rajesh Abraham Jacob Daniel Richard Hassaan Maan Jennifer A. Aguiar Wael L. Demian Kaushal Baid Michael R. D'Agostino Jann Catherine Ang Tetyana Murdza Benjamin J.-M. Tremblay Sam Afkhami Mehran Karimzadeh Aaron T. Irving Lily Yip Mario Ostrowski Jeremy A. Hirota Robert Kozak Terence D. Capellini Matthew S. Miller Bo Wang Samira Mubareka Allison J. McGeer Andrew G. McArthur Andrew C. Doxey Karen Mossman Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses iScience Immunology Virology |
| author_facet |
Arinjay Banerjee Nader El-Sayes Patrick Budylowski Rajesh Abraham Jacob Daniel Richard Hassaan Maan Jennifer A. Aguiar Wael L. Demian Kaushal Baid Michael R. D'Agostino Jann Catherine Ang Tetyana Murdza Benjamin J.-M. Tremblay Sam Afkhami Mehran Karimzadeh Aaron T. Irving Lily Yip Mario Ostrowski Jeremy A. Hirota Robert Kozak Terence D. Capellini Matthew S. Miller Bo Wang Samira Mubareka Allison J. McGeer Andrew G. McArthur Andrew C. Doxey Karen Mossman |
| author_sort |
Arinjay Banerjee |
| title |
Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses |
| title_short |
Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses |
| title_full |
Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses |
| title_fullStr |
Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses |
| title_full_unstemmed |
Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses |
| title_sort |
experimental and natural evidence of sars-cov-2-infection-induced activation of type i interferon responses |
| publisher |
Elsevier |
| series |
iScience |
| issn |
2589-0042 |
| publishDate |
2021-05-01 |
| description |
Summary: Type I interferons (IFNs) are our first line of defense against virus infection. Recent studies have suggested the ability of SARS-CoV-2 proteins to inhibit IFN responses. Emerging data also suggest that timing and extent of IFN production is associated with manifestation of COVID-19 severity. In spite of progress in understanding how SARS-CoV-2 activates antiviral responses, mechanistic studies into wild-type SARS-CoV-2-mediated induction and inhibition of human type I IFN responses are scarce. Here we demonstrate that SARS-CoV-2 infection induces a type I IFN response in vitro and in moderate cases of COVID-19. In vitro stimulation of type I IFN expression and signaling in human airway epithelial cells is associated with activation of canonical transcriptions factors, and SARS-CoV-2 is unable to inhibit exogenous induction of these responses. Furthermore, we show that physiological levels of IFNα detected in patients with moderate COVID-19 is sufficient to suppress SARS-CoV-2 replication in human airway cells. |
| topic |
Immunology Virology |
| url |
http://www.sciencedirect.com/science/article/pii/S2589004221004454 |
| work_keys_str_mv |
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1721424557207715840 |
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doaj-7903286efe6640018b5c5ad804e712c62021-05-28T05:03:53ZengElsevieriScience2589-00422021-05-01245102477Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responsesArinjay Banerjee0Nader El-Sayes1Patrick Budylowski2Rajesh Abraham Jacob3Daniel Richard4Hassaan Maan5Jennifer A. Aguiar6Wael L. Demian7Kaushal Baid8Michael R. D'Agostino9Jann Catherine Ang10Tetyana Murdza11Benjamin J.-M. Tremblay12Sam Afkhami13Mehran Karimzadeh14Aaron T. Irving15Lily Yip16Mario Ostrowski17Jeremy A. Hirota18Robert Kozak19Terence D. Capellini20Matthew S. Miller21Bo Wang22Samira Mubareka23Allison J. McGeer24Andrew G. McArthur25Andrew C. Doxey26Karen Mossman27Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada; Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; McMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Corresponding authorMcMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S 4K1, CanadaInstitute of Medical Science, University of Toronto, Toronto, ON M5S 1A8, CanadaDepartment of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada; Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; McMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, CanadaDepartment of Human Evolutionary Biology, Harvard University, Cambridge, MA 02138, USAVector Institute for Artificial Intelligence, Toronto, ON M5G 1M1, Canada; Peter Munk Cardiac Centre, University Health Network, Toronto, ON M5G 2C4, CanadaDepartment of Biology, University of Waterloo, Waterloo, ON N2L 3G1, CanadaDepartment of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada; Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; McMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, CanadaMcMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S 4K1, CanadaMichael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; McMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S 4K1, CanadaMichael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; McMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S 4K1, CanadaMcMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S 4K1, CanadaDepartment of Biology, University of Waterloo, Waterloo, ON N2L 3G1, CanadaMichael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; McMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S 4K1, CanadaVector Institute for Artificial Intelligence, Toronto, ON M5G 1M1, CanadaZhejiang University – University of Edinburgh Institute, Haining, Zhejiang 314400, China; Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310027, ChinaSunnybrook Research Institute, Toronto, ON M4N 3M5, CanadaDepartment of Medicine, University of Toronto, Toronto, ON M5S 3H2, Canada; Keenan Research Centre for Biomedical Science of St. Michael's Hospital, UnityHealth, Toronto, ON M5B 1W8, CanadaMichael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; Division of Respirology, Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada; Division of Respiratory Medicine, The University of British Columbia, Vancouver, BC V5Z 1M9, CanadaSunnybrook Research Institute, Toronto, ON M4N 3M5, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, CanadaDepartment of Human Evolutionary Biology, Harvard University, Cambridge, MA 02138, USAMichael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; McMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S 4K1, CanadaVector Institute for Artificial Intelligence, Toronto, ON M5G 1M1, Canada; Peter Munk Cardiac Centre, University Health Network, Toronto, ON M5G 2C4, Canada; Department of Computer Science, University of Toronto, Toronto, ON M5S 2E4, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, CanadaSunnybrook Research Institute, Toronto, ON M4N 3M5, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, CanadaMount Sinai Hospital, Toronto, ON M5G 1X5, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON M5S 1A1, CanadaMichael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON L8S 4K1, CanadaMichael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; Department of Biology, University of Waterloo, Waterloo, ON N2L 3G1, CanadaDepartment of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada; Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, ON L8S 4K1, Canada; McMaster Immunology Research Centre, McMaster University, Hamilton, ON L8S 4K1, Canada; Corresponding authorSummary: Type I interferons (IFNs) are our first line of defense against virus infection. Recent studies have suggested the ability of SARS-CoV-2 proteins to inhibit IFN responses. Emerging data also suggest that timing and extent of IFN production is associated with manifestation of COVID-19 severity. In spite of progress in understanding how SARS-CoV-2 activates antiviral responses, mechanistic studies into wild-type SARS-CoV-2-mediated induction and inhibition of human type I IFN responses are scarce. Here we demonstrate that SARS-CoV-2 infection induces a type I IFN response in vitro and in moderate cases of COVID-19. In vitro stimulation of type I IFN expression and signaling in human airway epithelial cells is associated with activation of canonical transcriptions factors, and SARS-CoV-2 is unable to inhibit exogenous induction of these responses. Furthermore, we show that physiological levels of IFNα detected in patients with moderate COVID-19 is sufficient to suppress SARS-CoV-2 replication in human airway cells.http://www.sciencedirect.com/science/article/pii/S2589004221004454ImmunologyVirology |