Abstract
It is well-known that viruses activate various inflammasomes, which can initiate the programmed cell death pathway known as pyroptosis, subsequently leading to cell lysis and release of inflammatory cytokines IL-1β and IL-18. This pathway can be triggered by various sensors, including, but not limited to, NLRP3, AIM2, IFI16, RIG-I, and NLRC4. Many viruses are known either to activate or inhibit inflammasomes as a part of the innate immune response or as a mechanism of pathogenesis. Early research in the field of virus-induced pyroptosis suggested a dichotomy, with RNA viruses activating the NLRP3 inflammasome and DNA viruses activating the AIM2 inflammasome. More recent research has shown that this dichotomy may not be as distinct as once thought. It seems many viruses activate multiple inflammasome sensors. Here, we detail which viruses fit the dichotomy as well as many that appear to defy this clearly false dichotomy. It seems likely that most, if not all, viruses activate multiple inflammasome sensors, and future research should focus on expanding our understanding of inflammasome activation in a variety of tissue types as well as virus activation of multiple inflammasomes, challenging biases that stemmed from early literature in this field. Here, we review primarily research performed on human viruses but also include details regarding animal viruses whenever possible.