Viral suppressors of the RIG-I-mediated interferon response are pre-packaged in influenza virions

Swantje Liedmann, Eike R. Hrincius, Cliff Guy, Darisuren Anhlan, Rüdiger Dierkes, Robert Carter, Gang Wu, Peter Staeheli, Douglas R. Green, Thorsten Wolff, Jonathan A. McCullers, Stephan Ludwig () and Christina Ehrhardt
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Swantje Liedmann: Institute of Molecular Virology (IMV), Center for Molecular Biology of Inflammation (ZMBE), University of Muenster
Eike R. Hrincius: St. Jude Children’s Research Hospital
Cliff Guy: St. Jude Children’s Research Hospital
Darisuren Anhlan: Institute of Molecular Virology (IMV), Center for Molecular Biology of Inflammation (ZMBE), University of Muenster
Rüdiger Dierkes: Institute of Molecular Virology (IMV), Center for Molecular Biology of Inflammation (ZMBE), University of Muenster
Robert Carter: St. Jude Children’s Research Hospital
Gang Wu: St. Jude Children’s Research Hospital
Peter Staeheli: Institute of Virology, University Medical Center Freiburg
Douglas R. Green: St. Jude Children’s Research Hospital
Thorsten Wolff: Division of Influenza and Other Respiratory Viruses
Jonathan A. McCullers: St. Jude Children’s Research Hospital
Stephan Ludwig: Institute of Molecular Virology (IMV), Center for Molecular Biology of Inflammation (ZMBE), University of Muenster
Christina Ehrhardt: Institute of Molecular Virology (IMV), Center for Molecular Biology of Inflammation (ZMBE), University of Muenster

Nature Communications, 2014, vol. 5, issue 1, 1-8

Abstract: Abstract The type I interferon (IFN) response represents the first line of defence to invading pathogens. Internalized viral ribonucleoproteins (vRNPs) of negative-strand RNA viruses induce an early IFN response by interacting with retinoic acid inducible gene I (RIG-I) and its recruitment to mitochondria. Here we employ three-dimensional stochastic optical reconstruction microscopy (STORM) to visualize incoming influenza A virus (IAV) vRNPs as helical-like structures associated with mitochondria. Unexpectedly, an early IFN induction in response to vRNPs is not detected. A distinct amino-acid motif in the viral polymerases, PB1/PA, suppresses early IFN induction. Mutation of this motif leads to reduced pathogenicity in vivo, whereas restoration increases it. Evolutionary dynamics in these sequences suggest that completion of the motif, combined with viral reassortment can contribute to pandemic risks. In summary, inhibition of the immediate anti-viral response is ‘pre-packaged’ in IAV in the sequences of vRNP-associated polymerase proteins.

Date: 2014
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DOI: 10.1038/ncomms6645

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