The NS segment of an H5N1 highly pathogenic avian influenza virus (HPAIV) is sufficient to alter replication efficiency, cell tropism, and host range of an H7N1 HPAIV - Wikidata - wikimedia - TriplyDB

The NS segment of an H5N1 highly pathogenic avian influenza virus (HPAIV) is sufficient to alter replication efficiency, cell tropism, and host range of an H7N1 HPAIV

The NS segment of an H5N1 highly pathogenic avian influenza virus (HPAIV) is sufficient to alter replication efficiency, cell tropism, and host range of an H7N1 HPAIV

http://www.wikidata.org/entity/Q33614553

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Human H7N9 avian influenza virus infection: a review and pandemic risk assessment The Influenza A Virus Protein NS1 Displays Structural Polymorphism Interaction of avian influenza virus NS1 protein and nucleolar and coiled-body phosphoprotein 1 Influenza A virus infections in swine: pathogenesis and diagnosis.In Silico Prediction and Experimental Confirmation of HA Residues Conferring Enhanced Human Receptor Specificity of H5N1 Influenza A Viruses Virulence of a novel reassortant canine H3N2 influenza virus in ferret, dog and mouse models.Role of the B Allele of Influenza A Virus Segment 8 in Setting Mammalian Host Range and Pathogenicity.D225G mutation in hemagglutinin of pandemic influenza H1N1 (2009) virus enhances virulence in mice.In vitro and in vivo characterization of a novel H1N1/2009 influenza virus reassortant with an NS gene from a highly pathogenic H5N1 virus, isolated from a human.Characterization of an artificial swine-origin influenza virus with the same gene combination as H1N1/2009 virus: a genesis clue of pandemic strain.Reassortment of NS segments modifies highly pathogenic avian influenza virus interaction with avian hosts and host cells.Highly pathogenic H5N1 influenza viruses carry virulence determinants beyond the polybasic hemagglutinin cleavage site.Activation of c-jun N-terminal kinase upon influenza A virus (IAV) infection is independent of pathogen-related receptors but dependent on amino acid sequence variations of IAV NS1.Multifunctional adaptive NS1 mutations are selected upon human influenza virus evolution in the mouse.Efficient generation of recombinant influenza A viruses employing a new approach to overcome the genetic instability of HA segments.Exposure to a low pathogenic A/H7N2 virus in chickens protects against highly pathogenic A/H7N1 virus but not against subsequent infection with A/H5N1.The virulence of 1997 H5N1 influenza viruses in the mouse model is increased by correcting a defect in their NS1 proteins.Non-structural protein 1 of avian influenza A viruses differentially inhibit NF-κB promoter activation.Influenza virus-induced caspase-dependent enlargement of nuclear pores promotes nuclear export of viral ribonucleoprotein complexes.Double-stranded RNA-induced activation of activating protein-1 promoter is differentially regulated by the non-structural protein 1 of avian influenza A viruses.Avian influenza virus hemagglutinins H2, H4, H8, and H14 support a highly pathogenic phenotype The amazing innate immune response to influenza A virus infection.Influenza A Virus Virulence Depends on Two Amino Acids in the N-Terminal Domain of Its NS1 Protein To Facilitate Inhibition of the RNA-Dependent Protein Kinase PKR.H5N1 influenza virulence, pathogenicity and transmissibility: what do we know?Prevalence of the C-terminal truncations of NS1 in avian influenza A viruses and effect on virulence and replication of a highly pathogenic H7N1 virus in chickens NS reassortment of an H7-type highly pathogenic avian influenza virus affects its propagation by altering the regulation of viral RNA production and antiviral host response.Nanodiamond enhances immune responses in mice against recombinant HA/H7N9 protein.The NS segment of H5N1 avian influenza viruses (AIV) enhances the virulence of an H7N1 AIV in chickens.Influenza virus sequence feature variant type analysis: evidence of a role for NS1 in influenza virus host range restriction.Avian influenza virus NS1: A small protein with diverse and versatile functions.Implications of segment mismatch for influenza A virus evolution.NS Segment of a 1918 Influenza A Virus-Descendent Enhances Replication of H1N1pdm09 and Virus-Induced Cellular Immune Response in Mammalian and Avian Systems.Zoonotic Potential of Influenza A Viruses: A Comprehensive Overview

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P2860

The NS segment of an H5N1 highly pathogenic avian influenza virus (HPAIV) is sufficient to alter replication efficiency, cell tropism, and host range of an H7N1 HPAIV

http://www.wikidata.org/entity/Q33614553

description

2009 nî lūn-bûn

@nan

2009 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի դեկտեմբերին հրատարակված գիտական հոդված

@hy

2009年の論文

@ja

2009年論文

@yue

2009年論文

@zh-hant

2009年論文

@zh-hk

2009年論文

@zh-mo

2009年論文

@zh-tw

2009年论文

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Journal of Virology

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The NS segment of an H5N1 high ...... nd host range of an H7N1 HPAIV

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Bianca Dauber

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Christina Ehrhardt

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Dominique Brenner

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Jürgen A Richt

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Kangzhen Yu

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Katrin Högner

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Oliver Planz

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Stephan Pleschka

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Thorsten Wolff

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Wenjun Ma

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P2860

Influenza A virus NS1 protein binds p85beta and activates phosphatidylinositol-3-kinase signaling

Influenza A virus NS1 targets the ubiquitin ligase TRIM25 to evade recognition by the host viral RNA sensor RIG-I

Avian influenza A virus (H7N7) associated with human conjunctivitis and a fatal case of acute respiratory distress syndrome

The H5N1 influenza virus NS genes selected after 1998 enhance virus replication in mammalian cells

Mutant influenza viruses with a defective NS1 protein cannot block the activation of PKR in infected cells

Structural basis for suppression of a host antiviral response by influenza A virus

Influenza virus propagation is impaired by inhibition of the Raf/MEK/ERK signalling cascade.

The multifunctional NS1 protein of influenza A viruses

Influenza virus NS1 protein counteracts PKR-mediated inhibition of replication.

Cellular antiviral responses against influenza A virus are countered at the posttranscriptional level by the viral NS1A protein via its binding to a cellular protein required for the 3' end processing of cellular pre-mRNAS

P304

2122-2133

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scholarly article

P356

10.1128/JVI.01668-09

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4

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84

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2009-12-09T00:00:00Z

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40685028

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20007264

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2812369

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