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Importin-α7 is involved in the formation of Ebola virus inclusion bodies but is not essential for pathogenicity in mice

Authors

  • G. Gabriel
  • F. Feldmann
  • R. Reimer
  • S. Thiele
  • M. Fischer
  • E. Hartmann
  • M. Bader
  • H. Ebihara
  • T. Hoenen
  • H. Feldmann

Journal

  • Journal of Infectious Diseases

Citation

  • J Infect Dis 212 (Suppl 2): S316-S321

Abstract

  • Ebola virus (EBOV) protein 24 antagonizes the host interferon (IFN) response by hijacking select nuclear importin-{alpha} isoforms. Thereby, it blocks STAT1-mediated IFN-{alpha}/{beta} and IFN-{gamma} synthesis. However, owing to the lack of importin-{alpha} knockout animal models in the past, their role in EBOV pathogenesis remained largely unknown. Here, we demonstrate that importin-{alpha}7 is involved in the formation of EBOV inclusion bodies and replication. However, deletion of the gene encoding importin-{alpha}7 was not sufficient to increase survival rates among mice infected with EBOV.


DOI

doi:10.1093/infdis/jiv240