Nonetheless, the splenic viral titer of infected WT and IFN-γ-KO BALB/c mice differed on average only 5-fold, while both strains displayed very different HLH symptoms [13], indicating that increased disease severity may not be exclusively attributed toaugmented viral proliferation but may emanate from additional differences in immune activation and immunopathology. This evidence concerns the gene IFNG and hemophagocytic syndrome.