Virulence-associated substitution D222G in the hemagglutinin of 2009 pandemic influenza A(H1N1) virus affects receptor binding.
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Recently emerged swine influenza A virus (H2N3) causes severe pneumonia in Cynomolgus macaquesTransmission of influenza A virusesAcute respiratory distress syndrome induced by a swine 2009 H1N1 variant in miceStructural Characterization of the Hemagglutinin Receptor Specificity from the 2009 H1N1 Influenza PandemicMolecular Basis of the Receptor Binding Specificity Switch of the Hemagglutinins from both the 1918 and 2009 Pandemic Influenza A Viruses by a D225G SubstitutionThe M segment of the 2009 pandemic influenza virus confers increased neuraminidase activity, filamentous morphology, and efficient contact transmissibility to A/Puerto Rico/8/1934-based reassortant virusesOne health, multiple challenges: The inter-species transmission of influenza A virusInfluenza A virus transmission via respiratory aerosols or droplets as it relates to pandemic potentialReceptor specificity does not affect replication or virulence of the 2009 pandemic H1N1 influenza virus in mice and ferretsAvian influenza A viruses: from zoonosis to pandemicIdentification of critical residues in the hemagglutinin and neuraminidase of influenza virus H1N1pdm for vaccine virus replication in embryonated chicken eggsHost adaptation and transmission of influenza A viruses in mammalsTwo years after pandemic influenza A/2009/H1N1: what have we learned?New variants and age shift to high fatality groups contribute to severe successive waves in the 2009 influenza pandemic in Taiwan.A Role for Neutrophils in Viral Respiratory Disease.Analysis of adaptation mutants in the hemagglutinin of the influenza A(H1N1)pdm09 virus.Frequency of D222G haemagglutinin mutant of pandemic (H1N1) pdm09 influenza virus in Tunisia between 2009 and 2011.Virus-specific factors associated with zoonotic and pandemic potential.Virological Surveillance of Influenza Viruses during the 2008-09, 2009-10 and 2010-11 Seasons in Tunisia.Histopathological evaluation of the diversity of cells susceptible to H5N1 virulent avian influenza virusPB2-588I enhances 2009 H1N1 pandemic influenza virus virulence by increasing viral replication and exacerbating PB2 inhibition of beta interferon expression.Polymorphisms at residue 222 of the hemagglutinin of pandemic influenza A(H1N1)pdm09: association of quasi-species to morbidity and mortality in different risk categoriesEffects of a hemagglutinin D222G substitution on the pathogenicity of 2009 influenza A (H1N1) virus in mice.Circulating avian influenza viruses closely related to the 1918 virus have pandemic potential.Molecular determinants of influenza virus pathogenesis in mice.Hemagglutinin 222D/G polymorphism facilitates fast intra-host evolution of pandemic (H1N1) 2009 influenza A viruses.Mutations to PB2 and NP proteins of an avian influenza virus combine to confer efficient growth in primary human respiratory cells.The hemagglutinin of the influenza A(H1N1)pdm09 is mutating towards stability.Identification of amino acid substitutions supporting antigenic change of influenza A(H1N1)pdm09 viruses.Molecular Characterisation of the Haemagglutinin Glycan-Binding Specificity of Egg-Adapted Vaccine Strains of the Pandemic 2009 H1N1 Swine Influenza A Virus.Analysis of the Contrasting Pathogenicities Induced by the D222G Mutation in 1918 and 2009 Pandemic Influenza A VirusesDifferential Susceptibilities of Human Lung Primary Cells to H1N1 Influenza VirusesTransmission and pathogenicity of novel reassortants derived from Eurasian avian-like and 2009 pandemic H1N1 influenza viruses in mice and guinea pigs.Reduction of Neuraminidase Activity Exacerbates Disease in 2009 Pandemic Influenza Virus-Infected Mice.Evolutionary ecology of virus emergence.Influenza A virus transmission: contributing factors and clinical implications.Receptor specificity of subtype H1 influenza A viruses isolated from swine and humans in the United States.Improving the evidence base for decision making during a pandemic: the example of 2009 influenza A/H1N1.Highly pathogenic avian influenza virus H5N1 infects alveolar macrophages without virus production or excessive TNF-alpha induction.Influenza A viruses: new research developments.
P2860
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P2860
Virulence-associated substitution D222G in the hemagglutinin of 2009 pandemic influenza A(H1N1) virus affects receptor binding.
description
2010 nî lūn-bûn
@nan
2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Virulence-associated substitut ...... irus affects receptor binding.
@ast
Virulence-associated substitut ...... irus affects receptor binding.
@en
type
label
Virulence-associated substitut ...... irus affects receptor binding.
@ast
Virulence-associated substitut ...... irus affects receptor binding.
@en
prefLabel
Virulence-associated substitut ...... irus affects receptor binding.
@ast
Virulence-associated substitut ...... irus affects receptor binding.
@en
P2093
P2860
P50
P356
P1433
P1476
Virulence-associated substitut ...... irus affects receptor binding.
@en
P2093
Anice C Lowen
Björn Koel
Chris S Whittleston
David J Wales
Derek J Smith
Eefje J A Schrauwen
Jianqiang Ye
John Steel
Kyle H Sutherland-Cash
Salin Chutinimitkul
P2860
P304
11802-11813
P356
10.1128/JVI.01136-10
P50
P577
2010-09-15T00:00:00Z