We try to understand the mechanism by which viral infection at the mucosal
surface is recognized and how the recognition process is involved in the
generation of adaptive immunity. We have previously demonstrated that unlike
toll-like receptors and retinoic acid-inducible gene I (RIG-I)-like helicases
that recognize viral RNA, the NLR family, pyrin domain containing 3 (NLRP3)
senses disturbance of intracellular ionic concentration induced by the
expression of virus-encoded ion channels (viroporins) such as the influenza
A virus M2 protein and the encephalomyocarditis virus (EMCV) 2B protein.
Recently, we demonstrated that the nonstructural protein 1 (NS1) of influenza
A virus interacts with the NLRP3 to inhibit a NLRP3/ASC-induced single
speck formation required for full activation of inflammasomes and IL-1beta
secretion. These results provide a basis for understanding the viral pathogenesis
and developing effective vaccines against viral pathogens.
1) Activation of the NLRP3 inflammasome by viroporins