Differential use of importin-α isoforms governs cell tropism and host adaptation of influenza virus

Gülsah Gabriel (), Karin Klingel, Anna Otte, Swantje Thiele, Ben Hudjetz, Gökhan Arman-Kalcek, Martina Sauter, Tatiana Shmidt, Franziska Rother, Sigrid Baumgarte, Björn Keiner, Enno Hartmann, Michael Bader, George G. Brownlee, Ervin Fodor and Hans-Dieter Klenk
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Gülsah Gabriel: Heinrich-Pette-Institute, Leibniz Institute for Experimental Virology
Karin Klingel: Institute of Pathology, University Hospital Tübingen, Tübingen
Anna Otte: Heinrich-Pette-Institute, Leibniz Institute for Experimental Virology
Swantje Thiele: Heinrich-Pette-Institute, Leibniz Institute for Experimental Virology
Ben Hudjetz: Heinrich-Pette-Institute, Leibniz Institute for Experimental Virology
Gökhan Arman-Kalcek: Heinrich-Pette-Institute, Leibniz Institute for Experimental Virology
Martina Sauter: Institute of Pathology, University Hospital Tübingen, Tübingen
Tatiana Shmidt: Max-Delbrück-Centre for Molecular Medicine
Franziska Rother: Max-Delbrück-Centre for Molecular Medicine
Sigrid Baumgarte: Institute for Hygiene and Environment
Björn Keiner: Institute of Virology, Philipps-University Marburg
Enno Hartmann: Institute for Biology, University of Lübeck
Michael Bader: Max-Delbrück-Centre for Molecular Medicine
George G. Brownlee: Sir William Dunn School of Pathology, University of Oxford
Ervin Fodor: Sir William Dunn School of Pathology, University of Oxford
Hans-Dieter Klenk: Institute of Virology, Philipps-University Marburg

Nature Communications, 2011, vol. 2, issue 1, 1-7

Abstract: Abstract Influenza A viruses are a threat to humans due to their ability to cross species barriers, as illustrated by the 2009 H1N1v pandemic and sporadic H5N1 transmissions. Interspecies transmission requires adaptation of the viral polymerase to importin-α, a cellular protein that mediates transport into the nucleus where transcription and replication of the viral genome takes place. In this study, we analysed replication, host specificity and pathogenicity of avian and mammalian influenza viruses, in importin-α-silenced cells and importin-α-knockout mice, to understand the role of individual importin-α isoforms in adaptation. For efficient virus replication, the polymerase subunit PB2 and the nucleoprotein (NP) of avian viruses required importin-α3, whereas PB2 and NP of mammalian viruses showed importin-α7 specificity. H1N1v replication depended on both, importin-α3 and -α7, suggesting ongoing adaptation of this virus. Thus, differences in importin-α specificity are determinants of host range underlining the importance of the nuclear envelope in interspecies transmission.

Date: 2011
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DOI: 10.1038/ncomms1158

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