Selected article for: "EBOV GP rvsv infection and GP rvsv"
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_11
    Snippet: IFNγ inhibition requires signaling through the type II interferon receptor in mouse macrophages IFNγ signals through the type II IFN receptor, thereby activating JAK/STAT pathways and initiating the expression of many ISGs [28] . However, low concentrations of type I IFNs can enhance responses to type II IFN and high concentrations can inhibit [29] [30] [31] . To assess if the IFNγ antiviral effect on macrophages was independent of type I IFN .....
    Document: IFNγ inhibition requires signaling through the type II interferon receptor in mouse macrophages IFNγ signals through the type II IFN receptor, thereby activating JAK/STAT pathways and initiating the expression of many ISGs [28] . However, low concentrations of type I IFNs can enhance responses to type II IFN and high concentrations can inhibit [29] [30] [31] . To assess if the IFNγ antiviral effect on macrophages was independent of type I IFN receptor signaling, peritoneal macrophages were harvested from interferon α/β receptor knockout mice (IFNAR -/-) and cultured for 24 hours with M-CSF or M-CSF plus IFNγ prior to EBOV GP/rVSV infection. IFNγ treatment of BALB/c or C57BL/6 IFNAR -/macrophages inhibited virus infection (S3A and S3B Fig) , indicating that IFNγ does not require the presence of a functional type I IFN receptor for its antiviral effect. To verify that the IFNγ response required the type II receptor, C57BL/6 IFNγ receptor knockout (IFNγR -/-) peritoneal macrophages were harvested and stimulated with M-CSF or M-CSF plus IFNγ prior to infection. As expected, IFNγ treatment had no effect on EBOV GP/rVSV viral titers in IFNγR -/cells, indicating that the type II IFN receptor is required for IFNγ-mediated inhibition of virus infection (S3C Fig) .

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