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

Author

Listed:
  • Gülsah Gabriel

    (Heinrich-Pette-Institute, Leibniz Institute for Experimental Virology
    Sir William Dunn School of Pathology, University of Oxford
    Oxford
    Institute of Virology, Philipps-University Marburg)

  • 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
    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
    Oxford)

  • Ervin Fodor

    (Sir William Dunn School of Pathology, University of Oxford
    Oxford)

  • Hans-Dieter Klenk

    (Institute of Virology, Philipps-University Marburg
    Marburg)

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.

Suggested Citation

  • 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 &, 2011. "Differential use of importin-α isoforms governs cell tropism and host adaptation of influenza virus," Nature Communications, Nature, vol. 2(1), pages 1-7, September.
  • Handle: RePEc:nat:natcom:v:2:y:2011:i:1:d:10.1038_ncomms1158
    DOI: 10.1038/ncomms1158
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