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dc.contributor.authorOtte, Anna
dc.contributor.authorMarriott, Anthony C
dc.contributor.authorDreier, Carola
dc.contributor.authorDove, Brian
dc.contributor.authorMooren, Kyra
dc.contributor.authorKlingen, Thorsten R
dc.contributor.authorSauter, Martina
dc.contributor.authorThompson, Katy-Anne
dc.contributor.authorBennett, Allan
dc.contributor.authorKlingel, Karin
dc.contributor.authorvan Riel, Debby
dc.contributor.authorMcHardy, Alice C
dc.contributor.authorCarroll, Miles W
dc.contributor.authorGabriel, Gülsah
dc.date.accessioned2016-07-20T14:57:59Z
dc.date.available2016-07-20T14:57:59Z
dc.date.issued2016
dc.identifier.citationEvolution of 2009 H1N1 influenza viruses during the pandemic correlates with increased viral pathogenicity and transmissibility in the ferret model. 2016, 6:28583 Sci Repen
dc.identifier.issn2045-2322
dc.identifier.pmid27339001
dc.identifier.doi10.1038/srep28583
dc.identifier.urihttp://hdl.handle.net/10033/617268
dc.description.abstractThere is increasing evidence that 2009 pandemic H1N1 influenza viruses have evolved after pandemic onset giving rise to severe epidemics in subsequent waves. However, it still remains unclear which viral determinants might have contributed to disease severity after pandemic initiation. Here, we show that distinct mutations in the 2009 pandemic H1N1 virus genome have occurred with increased frequency after pandemic declaration. Among those, a mutation in the viral hemagglutinin was identified that increases 2009 pandemic H1N1 virus binding to human-like α2,6-linked sialic acids. Moreover, these mutations conferred increased viral replication in the respiratory tract and elevated respiratory droplet transmission between ferrets. Thus, our data show that 2009 H1N1 influenza viruses have evolved after pandemic onset giving rise to novel virus variants that enhance viral replicative fitness and respiratory droplet transmission in a mammalian animal model. These findings might help to improve surveillance efforts to assess the pandemic risk by emerging influenza viruses.
dc.language.isoenen
dc.titleEvolution of 2009 H1N1 influenza viruses during the pandemic correlates with increased viral pathogenicity and transmissibility in the ferret model.en
dc.typeArticleen
dc.contributor.departmentViral Zoonoses and Adaptation, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.en
dc.identifier.journalScientific reportsen
refterms.dateFOA2018-06-13T14:11:49Z
html.description.abstractThere is increasing evidence that 2009 pandemic H1N1 influenza viruses have evolved after pandemic onset giving rise to severe epidemics in subsequent waves. However, it still remains unclear which viral determinants might have contributed to disease severity after pandemic initiation. Here, we show that distinct mutations in the 2009 pandemic H1N1 virus genome have occurred with increased frequency after pandemic declaration. Among those, a mutation in the viral hemagglutinin was identified that increases 2009 pandemic H1N1 virus binding to human-like α2,6-linked sialic acids. Moreover, these mutations conferred increased viral replication in the respiratory tract and elevated respiratory droplet transmission between ferrets. Thus, our data show that 2009 H1N1 influenza viruses have evolved after pandemic onset giving rise to novel virus variants that enhance viral replicative fitness and respiratory droplet transmission in a mammalian animal model. These findings might help to improve surveillance efforts to assess the pandemic risk by emerging influenza viruses.


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