Effector-triggered immunity in mammalian antiviral defense.

SARS-CoV-2 viroporins and NSP5 protease activities are sensed by human cells to trigger inflammasome-mediated pyroptosis. Guard proteins monitor viral inhibition of host cell protein synthesis within barrier epithelia and contribute to antiviral defense against diverse viruses in human skin. A novel self-guarded signaling pathway induces IFNB expression when disrupted and contributes to antiviral defense against herpes simplex virus 1 in human monocytes. The role of effector-triggered immunity in mammalian host defense against virus infection is poorly characterized. However, recent studies have identified new ways by which host cells recognize viral effectors, highlighting the importance of this host defense strategy in antiviral immunity. Effector-triggered immunity (ETI) is a common defense strategy used by mammalian host cells that is engaged upon detection of the enzymatic activities of pathogen-encoded proteins or the effects of their expression on cellular homeostasis. However, in contrast to the effector-triggered responses engaged upon bacterial infection, much less is understood about the activation and consequences of these responses following viral infection. Several recent studies have identified novel mechanisms by which viruses engage ETI, highlighting the importance of these immune responses in antiviral defense. We summarize recent advances in understanding how mammalian cells sense virus-encoded effector proteins, the downstream signaling pathways that are triggered by these sensing events, and how viruses manipulate these pathways to become more successful pathogens. [ABSTRACT FROM AUTHOR]