Author: Rhein, Bethany A.; Powers, Linda S.; Rogers, Kai; Anantpadma, Manu; Singh, Brajesh K.; Sakurai, Yasuteru; Bair, Thomas; Miller-Hunt, Catherine; Sinn, Patrick; Davey, Robert A.; Monick, Martha M.; Maury, Wendy
Title: Interferon-? Inhibits Ebola Virus Infection Document date: 2015_11_12
ID: 10bu7iwg_29
Snippet: Our studies also suggest that IFNγ treatment does not specifically target EBOV, as it protected against our BSL2 recombinant virus EBOV GP/rVSV and, to a more modest degree, against VSV in mice lacking type I IFN signaling. However, the timing of IFNγ protection against wild-type EBOV and wild-type VSV differed. IFNγ treatment protected against VSV only when given prior to infection, whereas post-challenge treatment appeared somewhat more effi.....
Document: Our studies also suggest that IFNγ treatment does not specifically target EBOV, as it protected against our BSL2 recombinant virus EBOV GP/rVSV and, to a more modest degree, against VSV in mice lacking type I IFN signaling. However, the timing of IFNγ protection against wild-type EBOV and wild-type VSV differed. IFNγ treatment protected against VSV only when given prior to infection, whereas post-challenge treatment appeared somewhat more efficacious against EBOV than pre-challenge treatment. Recent studies demonstrate that some ISGs are solely synthesized during the first few hours following IFN stimulation, whereas others are expressed for longer periods of time [50] . The difference in timing of IFNγ protection against VSV versus EBOV suggests that ISGs responsible for protection may differ. Future studies are needed to explore this possibility. Since mice challenged with EBOV GP/rVSV were protected by IFNγ treatment at post challenge time points in a manner similar to EBOV, the difference in timing of protection may be related to the cell populations targeted by the two wild-type viruses.
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