Figure 1.

Mechanisms and consequences of inflammasome activation (Martinon et al., 2002; Shi J. et al., 2015). Once the viral particles are captured by TLRs, the associated antiviral genes begin to be transcribed and translated. For the NLRP3 inflammasome, dsRNA viruses induce K⁺ efflux, Ca2⁺ mobilization, and/or ROS or dTGN production to activate the NLRP3 inflammasome. The hNLRP1 inflammasome can be activated by RNA, viral nucleic acid, viral pathogen enzymes, and viral structural proteins. The AIM2 inflammasome can be activated by DNA or viral nucleic acid. Activated inflammasomes recruit and activate pro-caspase-1 to cleave the GSDMD, pro-IL-1β, and pro-IL-18. The C-terminal domain of gasdermin D can induce pyroptosis, resulting in the release of large amounts of pro-inflammatory cytokines and causing acute or chronic inflammation.