Norovirus Regulation by Host and Microbe Megan T. Baldridge, Holly Turula, Christiane E. Wobus  Trends in Molecular Medicine  Volume 22, Issue 12, Pages 1047-1059 (December 2016) DOI: 10.1016/j.molmed.2016.10.003 Copyright © 2016 Elsevier Ltd Terms and Conditions

Figure 1 Key Figure: Varied Interactions between Host, Bacteria, and Murine Norovirus (MNoV) (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. Abbreviations: 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. Trends in Molecular Medicine 2016 22, 1047-1059DOI: (10.1016/j.molmed.2016.10.003) Copyright © 2016 Elsevier Ltd Terms and Conditions