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_19
Snippet: Additional less well-characterized ISGs that were highly upregulated in our gene array studies were also assessed for their ability to directly control virus infection. Ectopic expression of GBP5, RARRES3 and VAMP5 resulted in significant inhibition of EBOV GP/rVSV ( Fig 4B) . Evaluation of these ISGs for their ability to inhibit EBOV demonstrated that they also effectively blocked EBOV, identifying these as novel ISGs that are likely important f.....
Document: Additional less well-characterized ISGs that were highly upregulated in our gene array studies were also assessed for their ability to directly control virus infection. Ectopic expression of GBP5, RARRES3 and VAMP5 resulted in significant inhibition of EBOV GP/rVSV ( Fig 4B) . Evaluation of these ISGs for their ability to inhibit EBOV demonstrated that they also effectively blocked EBOV, identifying these as novel ISGs that are likely important for the control of EBOV in IFNγ-treated cells. Surprisingly, expression of STAT1 only modestly inhibited EBOV GP/rVSV infection, likely because significant levels of STAT1 are constitutively expressed within these cells and control of STAT1 activity is primarily regulated by its phosphorylation status [41] [42] [43] . Certainly not all ISGs tested that were highly upregulated in our gene arrays inhibited virus replication; GBP4, IFIT3, IFI27 and C1S had no effect on EBOV GP/rVSV.
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