Figure 2.

PARPs regulate the RNA sensors-mediated antiviral innate immune responses. (A) ZAP inhibits Sindbis virus (SINV) and Japanese encephalitis virus (JEV) probably by enhancing the RIG-I signaling pathway. (B) PARP9 recognizes and binds to dsRNA from reovirus or poly(I:C) and subsequently binds to and activates the PI3K regulatory subunit p85, and then further triggers the downstream AKT3 activation to phosphorylate IRF3 and IRF7 for IFN-I production. (C) The infection of vesicular stomatitis virus (VSV), influenza virus, Newcastle disease virus (NDV), Sendai virus (SeV), encephalomyocarditis virus (EMCV), or herpes simplex virus-1 (HSV-1) could activate the aryl hydrocarbon receptor (AhR), which subsequently upregulates the expression of PARP7. PARP7 physically interacts with TBK1 and inhibits its activity by ADP-ribosylation, abolishing the antiviral IFN-I signaling pathway. Dashed lines indicate uncertain interactions or that the underlying mechanism is not known.