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 language | English (US) |
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Pages (from-to) | S316-S321 |
Journal | Journal of Infectious Diseases |
Volume | 212 |
DOIs | |
State | Published - Oct 1 2015 |
Keywords
- Ebola virus
- STAT1
- VP24
- importin-α
- inclusion bodies
- interferon
- pathogenicity
ASJC Scopus subject areas
- Immunology and Allergy
- Infectious Diseases