| Literature DB >> 26185094 |
Gülsah Gabriel1, Friederike Feldmann2, Rudolph Reimer3, Swantje Thiele3, Meike Fischer3, Enno Hartmann4, Michael Bader5, Hideki Ebihara6, Thomas Hoenen6, Heinz Feldmann6.
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.Entities:
Keywords: Ebola virus; STAT1; VP24; importin-α; inclusion bodies; interferon; pathogenicity
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Year: 2015 PMID: 26185094 PMCID: PMC4564549 DOI: 10.1093/infdis/jiv240
Source DB: PubMed Journal: J Infect Dis ISSN: 0022-1899 Impact factor: 5.226