About: Transcriptomic Characterization of the Novel Avian-Origin Influenza A (H7N9) Virus: Specific Host Response and Responses Intermediate between Avian (H5N1 and H7N7) and Human (H3N2) Viruses and Implications for Treatment Options

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About: Transcriptomic Characterization of the Novel Avian-Origin Influenza A (H7N9) Virus: Specific Host Response and Responses Intermediate between Avian (H5N1 and H7N7) and Human (H3N2) Viruses and Implications for Treatment Options Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Transcriptomic Characterization of the Novel Avian-Origin Influenza A (H7N9) Virus: Specific Host Response and Responses Intermediate between Avian (H5N1 and H7N7) and Human (H3N2) Viruses and Implications for Treatment Options
Creator	Josset, Laurence Zeng, Hui Kelly, Sara Buchmeier, Michael Katze, Michael Tumpey, Terrence
topic	covid:bfa1dab8c91f41f59df39489115a8b2e19e537bf#this
Source	Medline; PMC
abstract	A novel avian-origin H7N9 influenza A virus (IAV) emerged in China in 2013, causing mild to lethal human respiratory infections. H7N9 originated with multiple reassortment events between avian viruses and carries genetic markers of human adaptation. Determining whether H7N9 induces a host response closer to that with human or avian IAV is important in order to better characterize this emerging virus. Here we compared the human lung epithelial cell response to infection with A/Anhui/01/13 (H7N9) or highly pathogenic avian-origin H5N1, H7N7, or human seasonal H3N2 IAV. The transcriptomic response to H7N9 was highly specific to this strain but was more similar to the response to human H3N2 than to that to other avian IAVs. H7N9 and H3N2 both elicited responses related to eicosanoid signaling and chromatin modification, whereas H7N9 specifically induced genes regulating the cell cycle and transcription. Among avian IAVs, the response to H7N9 was closest to that elicited by H5N1 virus. Host responses common to H7N9 and the other avian viruses included the lack of induction of the antigen presentation pathway and reduced proinflammatory cytokine induction compared to that with H3N2. Repression of these responses could have an important impact on the immunogenicity and virulence of H7N9 in humans. Finally, using a genome-based drug repurposing approach, we identified several drugs predicted to regulate the host response to H7N9 that may act as potential antivirals, including several kinase inhibitors, as well as FDA-approved drugs, such as troglitazone and minocycline. Importantly, we validated that minocycline inhibited H7N9 replication in vitro, suggesting that our computational approach holds promise for identifying novel antivirals.
has issue date	2014-02-04(xsd:dateTime)
bibo:doi	10.1128/mbio.01102-13
bibo:pmid	24496798
has license	cc-by-nc-sa
sha1sum (hex)	bfa1dab8c91f41f59df39489115a8b2e19e537bf
schema:url	https://doi.org/10.1128/mbio.01102-13
resource representing a document's title	Transcriptomic Characterization of the Novel Avian-Origin Influenza A (H7N9) Virus: Specific Host Response and Responses Intermediate between Avian (H5N1 and H7N7) and Human (H3N2) Viruses and Implications for Treatment Options
has PubMed Central identifier	PMC3950506
has PubMed identifier	24496798
schema:publication	mBio
resource representing a document's body	covid:bfa1dab8c91f41f59df39489115a8b2e19e537bf#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/bfa1dab8c91f41f59df39489115a8b2e19e537bf
is schema:about of	named entity 'VIRUS' named entity 'H7N9' named entity 'EICOSANOID' named entity 'IN VITRO' named entity 'THROUGHPUT' named entity 'VIRULENCE' named entity 'CHINA' named entity 'MILD' named entity 'NOVEL' named entity 'REPLICATION' named entity 'ANTIVIRAL' named entity 'LETHAL' named entity 'THESE' named entity 'VIRUS' named entity 'CLOSEST' named entity 'TROGLITAZONE' named entity 'ORDER' named entity 'INCLUDING' named entity 'REDUCED' named entity 'HERE' named entity 'HAVE' named entity 'PROMISE' named entity 'DEVELOPMENT' named entity 'ADAPTATION' named entity 'CAUSING' named entity 'TO REGULATE' named entity 'DRUG' named entity 'FDA' named entity 'VIRUSES' named entity 'STRAIN' named entity 'INFLUENZA VIRUS' named entity 'INFECTION' named entity 'REPRESSION' named entity 'INFECT' named entity 'NEW' named entity 'THE CELL' named entity 'RESERVOIR' named entity 'OUR' named entity 'LUNG EPITHELIAL CELL' named entity 'RAPID' named entity 'ANTIVIRALS' named entity 'HUMANS' named entity 'H7N9' named entity 'response' named entity 'rapid' named entity 'H7N9' named entity 'H7N7' named entity 'compared' named entity 'causing' named entity 'avian' named entity 'Here' named entity 'IAV' named entity 'Anhui' named entity 'adaptation' named entity 'Virus' named entity 'NOVEL' named entity 'SIMILAR' named entity 'ANTIGEN PRESENTATION PATHWAY' named entity 'CYTOKINE ' named entity 'CELL CYCLE' named entity 'ITS' named entity 'RESPIRATORY INFECTIONS' named entity 'HUMAN' named entity 'HIGH' named entity 'ACCELERATE' named entity 'IDENTIFYING' named entity 'KINASE INHIBITORS' named entity 'GENETIC MARKERS' named entity 'MINOCYCLINE' named entity 'IDENTIFIED' named entity 'H3N2' named entity 'BUT' named entity 'POTENTIAL' named entity 'CELL RESPONSE'

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