The H5N1 influenza virus NS genes selected after 1998 enhance virus replication in mammalian cells - Test2 - elhamkhani - TriplyDB

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

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

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Shutoff of Host Gene Expression in Influenza A Virus and Herpesviruses: Similar Mechanisms and Common Themes Lessons from emergence of A/goose/Guangdong/1996-like H5N1 highly pathogenic avian influenza viruses and recent influenza surveillance efforts in southern China Human H7N9 avian influenza virus infection: a review and pandemic risk assessment Structural basis for suppression of a host antiviral response by influenza A virus Structure of NS1A effector domain from the influenza A/Udorn/72 virus A Transient Homotypic Interaction Model for the Influenza A Virus NS1 Protein Effector Domain The Influenza A Virus Protein NS1 Displays Structural Polymorphism Functions of the influenza A virus NS1 protein in antiviral defense Host adaptation and transmission of influenza A viruses in mammals Mutations to PB2 and NP proteins of an avian influenza virus combine to confer efficient growth in primary human respiratory cells.Genetic characterization of avian influenza viruses isolated in Israel during 2000-2006.Mutations in the NS1 C-terminal tail do not enhance replication or virulence of the 2009 pandemic H1N1 influenza A virus.Inefficient control of host gene expression by the 2009 pandemic H1N1 influenza A virus NS1 protein Virulence determinants of pandemic influenza viruses.Virulence and genetic compatibility of polymerase reassortant viruses derived from the pandemic (H1N1) 2009 influenza virus and circulating influenza A viruses.An influenza reassortant with polymerase of pH1N1 and NS gene of H3N2 influenza A virus is attenuated in vivo.Novel inhibitor of influenza non-structural protein 1 blocks multi-cycle replication in an RNase L-dependent manner.Human-Animal Interface: The Case for Influenza Interspecies Transmission.Distinctive interactions of the Arabidopsis homolog of the 30 kD subunit of the cleavage and polyadenylation specificity factor (AtCPSF30) with other polyadenylation factor subunits Enterovirus 71 3C protease cleaves a novel target CstF-64 and inhibits cellular polyadenylation Molecular determinants of adaptation of highly pathogenic avian influenza H7N7 viruses to efficient replication in the human host 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 Innate immune evasion strategies of influenza viruses Genomic and protein structural maps of adaptive evolution of human influenza A virus to increased virulence in the mouse.Critical role of constitutive type I interferon response in bronchial epithelial cell to influenza infection.Glycine 184 in nonstructural protein NS1 determines the virulence of influenza A virus strain PR8 without affecting the host interferon response.Influenza A virus NS1 gene mutations F103L and M106I increase replication and virulence.Highly pathogenic H5N1 influenza A virus strains provoke heterogeneous IFN-α/β responses that distinctively affect viral propagation in human cells.Protein clustering and RNA phylogenetic reconstruction of the influenza A [corrected] virus NS1 protein allow an update in classification and identification of motif conservation.Exploring naphthyl-carbohydrazides as inhibitors of influenza A viruses.PB2 segment promotes high-pathogenicity of H5N1 avian influenza viruses in mice.The virulence of 1997 H5N1 influenza viruses in the mouse model is increased by correcting a defect in their NS1 proteins.U4 at the 3' UTR of PB1 segment of H5N1 influenza virus promotes RNA polymerase activity and contributes to viral pathogenicity A complete map of potential pathogenicity markers of avian influenza virus subtype H5 predicted from 11 expressed proteins Fluorescence-Activated Cell Sorting-Based Analysis Reveals an Asymmetric Induction of Interferon-Stimulated Genes in Response to Seasonal Influenza A Virus Selective Degradation of Host RNA Polymerase II Transcripts by Influenza A Virus PA-X Host Shutoff Protein.Evolutionary recovery of a recombinant viral genome.Novel Bat Influenza Virus NS1 Proteins Bind Double-Stranded RNA and Antagonize Host Innate Immunity Inability of NS1 protein from an H5N1 influenza virus to activate PI3K/Akt signaling pathway correlates to the enhanced virus replication upon PI3K inhibition.Structural Basis for a Novel Interaction between the NS1 Protein Derived from the 1918 Influenza Virus and RIG-I.

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

http://www.wikidata.org/entity/Q24676166

description

2007 nî lūn-bûn

@nan

2007 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2007 թվականի օգոստոսին հրատարակված գիտական հոդված

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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name

The H5N1 influenza virus NS ge ...... replication in mammalian cells

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The H5N1 influenza virus NS ge ...... replication in mammalian cells

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The H5N1 influenza virus NS ge ...... replication in mammalian cells

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The H5N1 influenza virus NS ge ...... replication in mammalian cells

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The H5N1 influenza virus NS ge ...... replication in mammalian cells

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The H5N1 influenza virus NS ge ...... replication in mammalian cells

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The H5N1 influenza virus NS ge ...... replication in mammalian cells

@ast

The H5N1 influenza virus NS ge ...... replication in mammalian cells

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The H5N1 influenza virus NS ge ...... replication in mammalian cells

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Journal of Virology

P1476

The H5N1 influenza virus NS ge ...... replication in mammalian cells

@en

P2093

Jesper Marklund

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Karen Y Twu

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Rei-Lin Kuo

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Robert M Krug

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P2860

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

Sequence of the 1918 pandemic influenza virus nonstructural gene (NS) segment and characterization of recombinant viruses bearing the 1918 NS genes

Lack of transmission of H5N1 avian-human reassortant influenza viruses in a ferret model

The 3'-end-processing factor CPSF is required for the splicing of single-intron pre-mRNAs in vivo.

Re-emergence of fatal human influenza A subtype H5N1 disease

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

Influenza virus NS1 protein interacts with the cellular 30 kDa subunit of CPSF and inhibits 3'end formation of cellular pre-mRNAs

Characterization of an avian influenza A (H5N1) virus isolated from a child with a fatal respiratory illness

Molecular basis for high virulence of Hong Kong H5N1 influenza A viruses

Influenza A virus NS1 protein activates the phosphatidylinositol 3-kinase (PI3K)/Akt pathway by direct interaction with the p85 subunit of PI3K.

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8112-21

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scholarly article

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2267722

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10.1128/JVI.00006-07

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15

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81

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2007-08-01T00:00:00Z

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17522219

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P932

1951328

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