About: IRF1 Maintains Optimal Constitutive Expression of Antiviral Genes and Regulates the Early Antiviral Response

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About: IRF1 Maintains Optimal Constitutive Expression of Antiviral Genes and Regulates the Early Antiviral Response Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	IRF1 Maintains Optimal Constitutive Expression of Antiviral Genes and Regulates the Early Antiviral Response
Creator	Ozato, Keiko Zanoni, Ivan Panda, Debasis Xing, Junji Wack, Andreas Bachu, Mahesh Gjinaj, Erisa Novatt, Hilary Squire, Erica Broggi, Achille Rabin, Ronald
topic	covid:c3c25b9a548eebd5505b4f20d75fa99a08ab88dd#this
Source	PMC
abstract	Viral defense at mucosal sites depends on interferons (IFN) and IFN stimulated genes (ISGs), either of which may be constitutively expressed to maintain an “antiviral state” (AVS). However, the mechanisms that govern the AVS are poorly defined. Using a BEAS-2B respiratory epithelial cell line deficient in IRF1, we demonstrate higher susceptibility to infection with vesicular stomatitis virus (VSV) and influenza virus. IRF1-mediated restriction of VSV is IFN-independent, as blockade of types I and III IFNs and JAK-STAT signaling before infection did not affect VSV infection of either parent or IRF1 KO cells. Transcriptome analysis revealed that IRF1 regulates constitutive expression of ~300 genes, including antiviral ISGs: OAS2, BST2, and RNASEL and knockdown of any of these IRF1-dependent genes increased VSV infection. Additionally, IRF1 enhances rapid expression of IFNβ and IFNλ after stimulation with poly I:C and also regulates ISG expression. Mechanistically, IRF1 enhances recruitment of BRD4 to promotor-enhancer regions of ISGs for rapid expression and maintains levels of histone H3K4me1 for optimal constitutive expression. Finally, IRF1 also regulates constitutive expression of TLR2 and TLR3 and promotes signaling through these pattern recognition receptors (PRR). These data reveal multiple roles for IRF1 toward effective anti-viral responses by maintaining IFN-independent constitutive expression of anti-viral ISGs and supporting early IFN-dependent responses to PRR stimulation.
has issue date	2019-05-15(xsd:dateTime)
bibo:doi	10.3389/fimmu.2019.01019
bibo:pmid	31156620
has license	cc-by
sha1sum (hex)	c3c25b9a548eebd5505b4f20d75fa99a08ab88dd
schema:url	https://doi.org/10.3389/fimmu.2019.01019
resource representing a document's title	IRF1 Maintains Optimal Constitutive Expression of Antiviral Genes and Regulates the Early Antiviral Response
has PubMed Central identifier	PMC6529937
has PubMed identifier	31156620
schema:publication	Front Immunol
resource representing a document's body	covid:c3c25b9a548eebd5505b4f20d75fa99a08ab88dd#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/c3c25b9a548eebd5505b4f20d75fa99a08ab88dd
is schema:about of	named entity 'ANTIVIRAL' named entity 'stimulation' named entity 'IRF1' named entity 'expression' named entity 'antiviral' named entity 'expression' named entity 'IRF1' named entity 'Optimal' named entity 'Antiviral' named entity 'OPTIMAL' named entity 'GENES' named entity 'OAS2' named entity 'DATA' named entity 'AFFECT' named entity 'RNASEL' named entity 'STIMULATED' named entity 'STIMULATION' named entity 'EPITHELIAL CELL LINE' named entity 'INCLUDING' named entity 'CONSTITUTIVE EXPRESSION' named entity 'DEPENDENT' named entity 'DEFENSE' named entity 'DID' named entity 'PARENT' named entity 'RAPID' named entity 'MAINTAINING' named entity 'IFN' named entity 'ENHANCER' named entity 'EARLY' named entity 'BST2' named entity 'STATE' named entity 'THESE' named entity 'EXPRESSION' named entity 'SUPPORTING' named entity 'BRD4' named entity 'OPTIMAL' named entity 'RESPONSES' named entity 'INTERFERONS' named entity 'TO MAINTAIN' named entity 'TYPES' named entity 'REGIONS' named entity 'RESPIRATORY EPITHELIAL CELL' named entity 'POORLY DEFINED' named entity 'EFFECTIVE' named entity 'TLR3' named entity 'INDEPENDENT' named entity 'RESTRICTION' named entity 'USING' named entity 'EARLY' named entity 'SUSCEPTIBILITY TO INFECTION' named entity 'STAT SIGNALING' named entity 'CELLS' named entity 'ROLES' named entity 'EITHER' named entity 'RECRUITMENT' named entity 'IRF1' named entity 'ANTIVIRAL RESPONSE' named entity 'TRANSCRIPTOME ANALYSIS' named entity 'GENES' named entity 'HISTONE' named entity 'MAY BE' named entity 'H3K4ME1' named entity 'BLOCKADE' named entity 'BEAS-2B' named entity 'DEFICIENT' named entity 'SITES' named entity 'VIRAL' named entity 'LEVELS' named entity 'INFLUENZA VIRUS'

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