The pathological alterations of heart and brain were positively associated with blood levels of C3a (survivors vs. non-survivor: 401 vs. 2007 ng/mL) and HMGB1 (survivors vs. non-survivor: 57 vs. 1794 ng/mL) at 1 h post-BI, suggesting that early complement activation and HMGB1 release may represent the mechanism underlying the development of myocarditis and encephalitis in non-survivor. The gene discussed is HMGB1; the disease is viral encephalitis.