Viral infections predispose host cells to damage and necrosis, leading to innate immune response initiation by host pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) [23] and changes in a range of cytokines involved in the inflammatory response [33] including TNF-α, IL-1β, and IL6. The gene discussed is IL1B; the disease is viral infectious disease.