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

J Infect Dis. 2015 Oct 1;212 Suppl 2(Suppl 2):S316-21. doi: 10.1093/infdis/jiv240. Epub 2015 Jul 16.

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.

Keywords: Ebola virus; STAT1; VP24; importin-α; inclusion bodies; interferon; pathogenicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Chlorocebus aethiops
  • DNA Replication / genetics
  • Ebolavirus / genetics
  • Ebolavirus / metabolism
  • Ebolavirus / pathogenicity*
  • Hemorrhagic Fever, Ebola / metabolism*
  • Hemorrhagic Fever, Ebola / virology*
  • Inclusion Bodies, Viral / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Vero Cells
  • Viral Proteins / metabolism
  • Virulence / genetics
  • Virulence / physiology*
  • Virus Replication / genetics
  • alpha Karyopherins / metabolism*

Substances

  • Viral Proteins
  • alpha Karyopherins