Murine FH induced by MHV-3 is a recognized and validated model for studying host resistance/susceptibility to human hepatitis virus, and several studies have shown that BALB/c or C57BL/6 mice have an innate susceptibility to the infection [3, 4] . FGL2 has been proposed as a critical mediating factor of lethality in the MHV-3-induced FH mice due to the fact that it has the capacity to induce fibrinogen deposition, which in turn activates the coagulation cascades and induces procoagulant activity [5] . To clarify whether the tissue necrosis we observed in PD-1-deficient mice following infection was also mediated by FGL2, the expression of FGL2 was analyzed. Results showed that the expression of FGL2 was principally associated with CD31-positive endothelial cells, CD68-positive macrophages and CD11c-positive DCs. Surprisingly, significantly higher levels of FGL2 were observed after infection in all of PD-1-deficient organs, including the liver, thymus, spleen, lymph nodes, and serum than that in those from WT littermates. In addition, increased fibrinogen deposition was observed in the organs of PD-1-deficient mice. Although we currently have no direct data to evidence that FGL2 directly mediates the mortality of our PD-1-deficient mice, data from other researchers have clearly shown that FGL2 promoted mouse mortality in response to MHV-3 infection [5, 28, 29, 30] . Considering this, our results strongly indicate that the mortality of PD-1-deficient mice post-MHV-3 infection is due to the higher level of FGL2 secretion and increased fibrinogen deposition.