Author: Zivcec, Marko; Scholte, Florine E. M.; Spiropoulou, Christina F.; Spengler, Jessica R.; Bergeron, Éric
Title: Molecular Insights into Crimean-Congo Hemorrhagic Fever Virus Document date: 2016_4_21
ID: 0a20s62q_22
Snippet: NP may contribute to viral-mediated immune evasion. Multiple aspects of the mammalian antiviral response appear to target the NP, like the interferon (IFN)-stimulated antiviral gene MxA, which inhibits CCHFV replication [62] . Furthermore, NP is highly immunogenic and is the major target of both B and T cells in mammals [37, [74] [75] [76] [77] . The NP of LASV and related hantaviruses have been shown to function as IFN antagonists [69, 78] . How.....
Document: NP may contribute to viral-mediated immune evasion. Multiple aspects of the mammalian antiviral response appear to target the NP, like the interferon (IFN)-stimulated antiviral gene MxA, which inhibits CCHFV replication [62] . Furthermore, NP is highly immunogenic and is the major target of both B and T cells in mammals [37, [74] [75] [76] [77] . The NP of LASV and related hantaviruses have been shown to function as IFN antagonists [69, 78] . However, CCHFV NP does not suppress the IFN response to Sendai virus infection [67] , a model virus that strongly activates the innate immune responses to double stranded RNA (dsRNA). Structurally related arenavirus NPs possess a conserved 3 1 to 5 1 exonuclease activity specific to RNA, and this RNase activity suppresses the innate immune response to dsRNA [69] . In vitro, CCHFV NP has endonuclease activity, but appears to be restricted to DNA instead of RNA [67] .
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