Selected article for: "IFN expression and proinflammatory cytokine"

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_34
    Snippet: EBOV evades the host innate immune signaling pathways through impaired type I and type II IFN signaling, dysregulated proinflammatory cytokine expression and suppression of DC maturation and T-cell activation [65] [66] [67] . This immune dysregulation is thought to allow EBOV to gain the upper hand during the course of infection; however, a reduction in viral antigen by as little as 2-fold appears to be the difference between the host survival an.....
    Document: EBOV evades the host innate immune signaling pathways through impaired type I and type II IFN signaling, dysregulated proinflammatory cytokine expression and suppression of DC maturation and T-cell activation [65] [66] [67] . This immune dysregulation is thought to allow EBOV to gain the upper hand during the course of infection; however, a reduction in viral antigen by as little as 2-fold appears to be the difference between the host survival and death during EBOV infection [68, 69] . As our IFNγ treatment of EBOV infected mice as late as 24 hours following lethal challenge demonstrates effective control of viral load, IFNγ treatment likely assists in overcoming EBOV-induced impairment of immune function by activation and maturation of immune cells as well as eliciting ISGs, leading to reduced EBOV RNA production as well as perhaps innate immune control of other aspects of the EBOV life cycle.

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