Based on the results of our study, we hypothesize that TLR3 deficiency led to an impaired innate immune response and hence to unrestricted viral infection and replication in neurons, brain inflammation with infiltration of inflammatory CD11b+Ly6Chigh monocytes, production of proinflammatory cytokines, and increased permeability of the blood–brain barrier, as also described in TLR3-deficient mice infected with Japanese encephalitis virus, a neurotropic flavivirus that is very similar to WNV [56]. The gene discussed is ITGAM; the disease is viral infectious disease.