Consistently, viral infection would induce the rapid transcription of extrahepatic BA transporters and rate-limiting biosynthesis genes, as well as lead to the intracellular accumulation of BAs in macrophages, which promoted the activation of antiviral signaling via the TGR5-β-arrestin-SRC axis, implying the universal role of BA metabolism in antiviral innate immunity (10, 11). Here, GPBAR1 is linked to viral infectious disease.