Response of host inflammasomes to viral infection

• Specific inflammasome activation induced by different viral infections induces the maturation of caspases and interleukins to cause downstream immune responses.
• The NLRP3 inflammasome is activated by intracellular ionic imbalance induced by several viroporins.
• RIG-I is not only involved in the NF-κB signaling pathway but also forms the RIG-I inflammasome during RNA virus infection.
• Some viral components can inhibit inflammasome activation to escape host immune defense systems.

Inflammasomes are multiprotein complexes that induce downstream immune responses to specific pathogens, environmental stimuli, and host cell damage. Components of specific viruses activate different inflammasomes; for example, the influenza A virus M2 protein and encephalomyocarditis virus (EMCV) 2B protein activate the nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome, whereas viral double-stranded RNA (dsRNA) activates the retinoic acid inducible gene-I (RIG-I) inflammasome. Once activated in response to viral infection, inflammasomes induce the activation of caspases and the release of mature forms of interleukin-1β (IL-1β) and IL-18. Here we review the association between viral infection and inflammasome activation. Identifying the mechanisms underlying virus-induced inflammasome activation is important if we are to develop novel therapeutic strategies to target viruses.