MHV-3 is a single-stranded, positive-sense RNA virus that belongs to the Coronaviridae family. In inbred laboratory mice, the virus produces strain-dependent disease profiles that depend on the infection route, age, genetic background, and immune status of the host. For example, Balb/c, C57BL/6 and DBA/2 mice develop acute fulminant hepatitis, while C3H mice develop a mild chronic disease and mice of the A strain exhibit no evidence of hepatitis [3, 4] . In contrast to the resistant A strain mice, FH induced by MHV-3 in susceptible mice is characterized by the presence of sinusoidal thrombosis and hepatocellular necrosis [2, 3] . These pathological findings occur concomitantly with expression of fibrinogen-like protein 2 (FGL2), a virus-induced procoagulant molecule in the sinusoidal lining cells in the liver. FGL2 has the capacity to promote fibrinogen deposition and subsequently directly induce the coagulation cascades by the expression of procoagulant activity (PCA) [5] . Thus, up-regulation of FGL2 is an essential component of the lethal effects of MHV-3-induced FH.