After infection, the virus evades the host’s immune system and causes brain and central nervous system (CNS) inflammation through several recognition receptors, such as Toll-like receptor 3 (TLR-3; an endosomal receptor for dsRNA of the rabies virus during replication), TLR-7 (a receptor for ssRNA), and retinoic acid-inducible gene I-like receptors (RIG-I; a cytosolic receptor for most dsRNA and some ssRNA) [4]. This evidence concerns the gene TLR3 and infection.