摘要Objective? To explore the role of MyD88 signaling in MHV-3 virus-mediated fulminant hepatitis. Methods? We evaluated liver lesion status, the expression of multiple pro-inflammatory cytokines and HMGB1, the recruitment of inflammatory ILC3, and mortality in MyD88-/-and WT mice. Results? The expression of multiple pro-inflammatory cytokines that recruit inflammatory ILC3 to the liver was severely impaired in MyD88-/- mice resulting in reduced liver pathology, viral replication, and mortality post-infection. Additionally, MHV-3 markedly increased the expression of high-mobility group box 1 (HMGB1) in infected hepatocytes/macrophages and induced HMGB1 protein migration from the nucleus to the extracellular milieu, where it activates MyD88-dependent inflammation. Conclusion? Our findings indicate that MyD88 exacerbates immunological pathology in experimental viral fulminant hepatitis.