Regulation of innate immune responses by cell death-associated caspases during virus infection.

Abstract

Viruses are obligate intracellular pathogens that rely on the cellular machinery for successful replication and dissemination. The host cells encode a number of different strategies to sense and restrict the invading viral pathogens. Caspase-mediated programmed cell death pathways that are triggered by virus infection, such as apoptosis and pyroptosis, are means for the infected cells to limit viral proliferation, leading to suicidal cell death (apoptosis) or lytic cell death to alert uninfected cells to mount anti-viral responses (pyroptosis). However, some viruses can employ the activated caspases to dampen the anti-viral responses to facilitate viral replication through cleavage of critical molecules of the innate immune pathways. The regulation of innate immune responses by caspases activation during virus infection has recently become an important topic. In this review, we will briefly introduce the characteristics of different classes of caspases and the cell death pathways regulated by these caspases. We will then describe how viruses trigger or dampen caspase activation during infection and how these activated caspases regulate three major innate immune response pathways of viral infections: the RLR, TLR and cGAS-STING pathways.