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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Trends Mol Med. 2016 Nov 22;22(12):1047–1059. doi: 10.1016/j.molmed.2016.10.003

Figure 1.

Figure 1

(A) Commensal bacteria facilitate persistent MNoV infection in a manner counteracted by innate immune factors IRF3, IFNLR1, and STAT1. (B) Commensal bacteria and MNoV are both needed to drive TNF-α and IFN-γ-mediated intestinal inflammation in mice lacking Atg16l1 or Il10. (C) MNoV exacerbates intestinal inflammation and lethality during pathogenic bacterial infection by potentiating inflammatory signals, including TNF-α and type I IFN, and host responses to bacteria. (D) In the absence of commensal bacteria, MNoV may replace protective functions of enteric microbes via type I IFN signaling. (E) In other contexts, MNoV can serve a protective role by decreasing the host inflammatory response to bacterial pathogens. IFN, interferon; IFNLR1, interferon λ receptor 1; IL, interleukin; IRF3, interferon regulatory transcription factor 3; NOD, nucleotide-binding oligomerization domain; STAT1, signal transducer and activator of transcription 1; TNF, tumor necrosis factor.