Race between virus and inflammasomes: inhibition or escape, intervention and therapy

Abstract

The inflammasome is a multiprotein complex that further regulates cell pyroptosis and inflammation by activating caspase-1. The assembly and activation of inflammasome are associated with a variety of diseases. Accumulative studies have shown that inflammasome is a key modulator of the host’s defense response to viral infection. Indeed, it has been established that activation of inflammasome occurs during viral infection. At the same time, the host has evolved a variety of corresponding mechanisms to inhibit unnecessary inflammasome activation. Therefore, here, we review and summarize the latest research progress on the interaction between inflammosomes and viruses, highlight the assembly and activation of inflammosome in related cells after viral infection, as well as the corresponding molecular regulatory mechanisms, and elucidate the effects of this activation on virus immune escape and host innate and adaptive immune defenses. Finally, we also discuss the potential therapeutic strategies to prevent and/or ameliorate viral infection-related diseases via targeting inflammasomes and its products.

Advances in the mechanism of inflammasomes activation in herpes virus infection

“…The self-cleavage of caspase-1 leads to the production of active caspase-1 p10/p20 tetramers. Subsequently, activated caspase-1 cleaves the inactive pre-forms of IL-1β and IL-18 to secrete these cytokines ( 95 ). The essential role of IFI16 or ASC in virus-induced caspase-1 processing was demonstrated using short hairpin RNA (shRNA) targeting them.Previously, IFI16 was not considered as an inflammasome activator due to its inability to constructively activate the inflammasome when overexpressed, unlike AIM2 function ( 77 ).…”