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pubmed-article:21035159pubmed:abstractTextType I interferons (IFNs) are essential to the clearance of viral diseases, however, a clear distinction between genes upregulated by direct virus-cell interactions and genes upregulated by secondary IFN production has not been made. Here, we investigated differential gene regulation in ferrets upon subcutaneous administration of IFN-?2b and during SARS-CoV infection. In vivo experiments revealed that IFN-?2b causes STAT1 phosphorylation and upregulation of abundant IFN response genes (IRGs), chemokine receptors, and other genes that participate in phagocytosis and leukocyte transendothelial migration. During infection with SARS-CoV not only a variety of IRGs were upregulated, but also a significantly broader range of genes involved in cell migration and inflammation. This work allowed dissection of several molecular signatures present during SARS-CoV which are part of a robust IFN antiviral response. These signatures can be useful markers to evaluate the status of IFN responses during a viral infection and specific features of different viruses.lld:pubmed
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pubmed-article:21035159pubmed:copyrightInfoCopyright © 2010 Elsevier Inc. All rights reserved.lld:pubmed
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pubmed-article:21035159pubmed:articleTitleEarly gene expression events in ferrets in response to SARS coronavirus infection versus direct interferon-alpha2b stimulation.lld:pubmed
pubmed-article:21035159pubmed:affiliationDivision of Experimental Therapeutics, Toronto General Research Institute, University Health Network, 101 College Street, Toronto, Ontario, Canada.lld:pubmed
pubmed-article:21035159pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21035159pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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