Our finding is consistent with the results from previous studies suggesting a role for pathogenic Th17 cells and CD4+ and CD8+ T cells in fatal SVNI encephalitis.67-69 Thus, the protection observed in GZ-161-treated mice could result directly from the suppression of cytotoxic and detrimental immune response pathways activated by SVNI and not from a reduction in viral replication. The gene discussed is CD8A; the disease is viral encephalitis.