This conclusion is consistent with previous studies showing that the primary target of SVNI is the brain and that the ability of SVNI to spread to the CNS is the cause of fatal disease.39 In addition, while GZ-161 significantly improved the survival rate of the mice, GZ-346, which cannot penetrate the brain (35), had no effect when administered beginning 2 days post-SVNI infection (data not shown), which suggested that the inhibition of UGCG in the brain is necessary for therapeutic effects. This evidence concerns the gene UGCG and infection.