Experiments with antibodies that block the functions of the pro-inflammatory cytokines that were differentially expressed in serum of WNV-infected anti-IFNAR1-treated SPF and GF mice could address this question; and (d) we have not linked the mechanism of disease severity associated with defects in type I IFN signaling identified in mice with that of human patients having auto-Abs to IFNs and WNV encephalitis. Here, IFNAR1 is linked to encephalitis.