The inflammasome is part of the innate immune system that regulates effector cells during inflammation [104–107]. Inflammasomes are cytosolic protein complexes consisting of multiple oligomeric molecules that detect cell-damaging agents and pathogenic factors by recognizing danger-associated molecular patterns (DAMP) and pathogen-associated molecular patterns (PAMP), respectively [104]. Through cleavage of pro-IL-1β and pro-IL-18, they promote the secretion of the active forms of IL-1β and IL-18. Long-term exposure of the host to viruses causes dysregulated inflammation and autoinflammatory disorders. Activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome is triggered by viral replication and leads to the destruction of viruses [105]. The murine coronavirus mouse hepatitis virus (MHV) activates NLRP3 inflammasomes and induces proinflammatory programmed cell death by panoptosis (pyroptosis, apoptosis, and necroptosis) [106,107]. The deleterious effects on the host due to inflammasome impairment indicate that balanced regulation of inflammasomes is crucial for the immune response and antiviral defense.