Further, our observations that NLRP3 signaling is important for limiting lethality and tissue destruction during WNV infection in vivo is consistent with models of influenza infection which have also shown a requirement for NLRP3 and IL-1β signaling in protective immunity against the virus [32], [34], [36] as well as in limiting collagen deposition and necrosis of lung tissue [34] and thus demonstrate a broad range for NLRP3 signaling in immunity to virus infection. This evidence concerns the gene IL1B and viral infectious disease.