Please use this identifier to cite or link to this item:
http://hdl.handle.net/11375/26588
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DC Field | Value | Language |
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dc.contributor.author | Banerjee A | - |
dc.contributor.author | El-Sayes N | - |
dc.contributor.author | Budylowski P | - |
dc.contributor.author | Jacob RA | - |
dc.contributor.author | Richard D | - |
dc.contributor.author | Maan H | - |
dc.contributor.author | Aguiar JA | - |
dc.contributor.author | Demian WL | - |
dc.contributor.author | Baid K | - |
dc.contributor.author | D'Agostino MR | - |
dc.contributor.author | Ang JC | - |
dc.contributor.author | Murdza T | - |
dc.contributor.author | Tremblay BJ-M | - |
dc.contributor.author | Afkhami S | - |
dc.contributor.author | Karimzadeh M | - |
dc.contributor.author | Irving AT | - |
dc.contributor.author | Yip L | - |
dc.contributor.author | Ostrowski M | - |
dc.contributor.author | Hirota JA | - |
dc.contributor.author | Kozak R | - |
dc.contributor.author | Capellini TD | - |
dc.contributor.author | Miller MS | - |
dc.contributor.author | Wang B | - |
dc.contributor.author | Mubareka S | - |
dc.contributor.author | McGeer AJ | - |
dc.contributor.author | McArthur AG | - |
dc.contributor.author | Doxey AC | - |
dc.contributor.author | Mossman K | - |
dc.date.accessioned | 2021-06-15T15:39:57Z | - |
dc.date.available | 2021-06-15T15:39:57Z | - |
dc.date.issued | 2021-05 | - |
dc.identifier.issn | 2589-0042 | - |
dc.identifier.issn | 2589-0042 | - |
dc.identifier.uri | http://hdl.handle.net/11375/26588 | - |
dc.description.abstract | 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. | - |
dc.publisher | Elsevier BV | - |
dc.rights | Attribution-NonCommercial-NoDerivs - CC BY-NC-ND This license is the most restrictive of the main Creative Commons licenses, only allowing others to download your works and share them with others as long as they credit you, but they can?t change them in any way or use them commercially. | - |
dc.rights.uri | 7 | - |
dc.subject | Immunology | - |
dc.subject | Virology | - |
dc.title | Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses | - |
dc.type | Article | - |
dc.date.updated | 2021-06-15T15:39:54Z | - |
dc.rights.license | Attribution-NonCommercial-NoDerivs - CC BY-NC-ND | - |
dc.identifier.doi | https://doi.org/10.1016/j.isci.2021.102477 | - |
Appears in Collections: | Faculty Publications (via McMaster Experts) |
Files in This Item:
File | Description | Size | Format | |
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Experimental and natural evidence of SARS-CoV-2-infection-induced activation of type I interferon responses.pdf | Published version | 4.13 MB | Adobe PDF | View/Open |
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