We propose a model for virus-induced sepsis-like syndrome (Fig. 9) in which infection in myeloid cells results in excessive viral RNA production, RIG-I and/or MDA5 recognition, MAVS signaling, NF-κB activation, proinflammatory cytokine production (including TNF-α), complement protein induction, alternative pathway activation, and complement anaphylatoxin production. Here, NFKB1 is linked to infection.