MAVS and herpes simplex encephalitis: However, deletion of Toll-interleukin-1 receptor (TIR) domain-containing adapter protein-inducing interferon beta (TRIF) and mitochondrial antiviral signaling protein (MAVS), which inactivates Toll-like receptor (TLR) 3 (TLR3) and RIG-I-like receptor (RLR) signaling, respectively, renders mice more susceptible to HSV-1 infection, and infected mice exhibit a phenotype resembling in many aspects that of HSE patients with inborn errors in the TLR3 axis [22].