Importin-α7 Is Involved in the Formation of Ebola Virus Inclusion Bodies but Is Not Essential for Pathogenicity in Mice

Gülsah Gabriel, Friederike Feldmann, Rudolph Reimer, Swantje Thiele, Meike Fischer, Enno Hartmann, Michael Bader, Hideki Ebihara, Thomas Hoenen, Heinz Feldmann

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Ebola virus (EBOV) protein 24 antagonizes the host interferon (IFN) response by hijacking select nuclear importin-α isoforms. Thereby, it blocks STAT1-mediated IFN-α/β and IFN-γ synthesis. However, owing to the lack of importin-α knockout animal models in the past, their role in EBOV pathogenesis remained largely unknown. Here, we demonstrate that importin-α7 is involved in the formation of EBOV inclusion bodies and replication. However, deletion of the gene encoding importin-α7 was not sufficient to increase survival rates among mice infected with EBOV.

Original languageEnglish (US)
Pages (from-to)S316-S321
JournalJournal of Infectious Diseases
Volume212
DOIs
StatePublished - Oct 1 2015

Keywords

  • Ebola virus
  • STAT1
  • VP24
  • importin-α
  • inclusion bodies
  • interferon
  • pathogenicity

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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    Gabriel, G., Feldmann, F., Reimer, R., Thiele, S., Fischer, M., Hartmann, E., Bader, M., Ebihara, H., Hoenen, T., & Feldmann, H. (2015). Importin-α7 Is Involved in the Formation of Ebola Virus Inclusion Bodies but Is Not Essential for Pathogenicity in Mice. Journal of Infectious Diseases, 212, S316-S321. https://doi.org/10.1093/infdis/jiv240