Our result showing that activated microglia reduce HSV-1 infectivity is consistent with previous findings of robust expression of antiviral mediators, such as TNF-α and CXCL10, in both mouse and human primary microglia stimulated with HSV-1 during nonproductive infection [27,28], as TNF-α and CXCL10 reduce HSV-1 replication in permissive cells [27]. This evidence concerns the gene CXCL10 and infection.