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. 2018 Oct 10;7:167. doi: 10.1038/s41426-018-0168-0

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a Type I IFN signaling inhibition (blue): NS2a, NS4a, and NS4b complex inhibit signal transducer and activator of transcription 1 (STAT1) signaling after IFNα/β receptor activation. NS5 will cause proteasomal degradation of STAT2 by binding with the host ubiquitin protein ligase E3 component N-recognin 4 (UBR4). b Complement evasion (red): NS1 hexamer inhibits the formation of the classical pathway C3 convertase by binding to C4, C1s, and C4b. NS1 inhibits neutralization by the mannose-binding lectin (MBL) pathway by binding to MBL. NS1 blocks membrane attack complex (MAC) formation by binding to complement regulators vitronectin (VN), C9, or clusterin (Clu)