Some in vivo data may support this hypothesis: several reports indicate that impaired IFN responses in vivo can result in uncontrolled lytic virus replication and, often fatal, afflictions of the central nervous system, including herpes simplex encephalitis in humans [43], [44], and increased replication efficiency of strongly attenuated HSV-1 mutants in TG neurons of mice [45]. This evidence concerns the gene IFNA1 and herpes simplex encephalitis.