Infectious bronchitis virus accessory protein 3a induces renal inflammatory injury by activating the NLRP3 inflammasome via ER calcium mobilization and mitochondrial ROS production

release and promotes accumulation of mitochondrial reactive oxygen species (mtROS), thereby enhancing NLRP3 inflammasome activation. These findings indicate that IBV 3a is a critical mediator of NLRP3-dependent inflammatory activation, advance our understanding of IBV renal pathogenesis, and provide a rationale and potential targets for the design of gene-deletion attenuated IBV vaccines.