Functional failure of TLR3 and its signaling components contribute to herpes simplex encephalitis.

Herpes simplex encephalitis (HSE) is a severe neurological disease in children and adults caused by herpes simplex virus. This review discusses recent findings on the role of Toll-like receptor 3 (TLR3) deficiencies in the HSE development. Critical checkpoints in the TLR3 signaling that contribute to innate response are discussed, including the importance of TLR3 ligand recognition site and transportation in the cell. We also indicate unresolved issues in the TLR3 functioning that might lead to thorough understanding of immunity during HSE. Such a knowledge base will lead to discovery and design of a rationale therapeutic and preventive approach against HSE.