Abstract
Influenza A virus (IAV) infection of epithelial cells activates NF-κB transcription factors via the canonical NF-κB signaling pathway, which modulates both the antiviral immune response and viral replication. Since almost nothing is known so far about a function of noncanonical NF-κB signaling after IAV infection, we tested infected cells for activation of p52 and RelB. We show that the viral NS1 protein strongly inhibits RIG-I-mediated noncanonical NF-κB activation and expression of the noncanonical target gene CCL19.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line
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DEAD Box Protein 58
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DEAD-box RNA Helicases / antagonists & inhibitors*
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DEAD-box RNA Helicases / metabolism
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Epithelial Cells / metabolism
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Epithelial Cells / virology
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Gene Expression
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Host-Pathogen Interactions / genetics
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Host-Pathogen Interactions / immunology
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Host-Pathogen Interactions / physiology
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Humans
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Influenza A virus / pathogenicity
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Influenza A virus / physiology*
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Lung / metabolism
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Lung / virology
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NF-kappa B / metabolism*
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NF-kappa B p52 Subunit / metabolism
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Receptors, Immunologic
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Signal Transduction
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Transcription Factor RelB / metabolism
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Viral Nonstructural Proteins / physiology*
Substances
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INS1 protein, influenza virus
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NF-kappa B
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NF-kappa B p52 Subunit
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RELB protein, human
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Receptors, Immunologic
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Viral Nonstructural Proteins
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Transcription Factor RelB
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RIGI protein, human
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DEAD Box Protein 58
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DEAD-box RNA Helicases