FIG 3.

Bile acids elicit their antiviral activity independently of FXR, vitamin D receptor, and IFNAR1. (A) Primary hepatocytes of FXR knockout and wild-type control mice were incubated with 25 μM TCDC or GW4064 for 3 h and subsequently infected with Δm157-MCMV-luciferase (0.1 PFU/cell) for the next 24 h before luciferase activity was measured. (B) Primary mouse hepatocytes were incubated for 24 h with 5 μM calcifediol or 0,5 μM calcitriol before being infected with Δm157-MCMV:luciferase (PFU:0.1). Luciferase activity was quantitated at 24 h after infection. (C) Primary mouse hepatocytes were conditioned for 24 h with 500 U/ml IFN-α, 500 U/ml IFN-γ, or a combination of both and, if indicated, for a further 3 h with 25 μM TCDC before the cells were infected with Δm157-MCMV-luciferase (0.1 PFU/cell) for an additional 24 h. Cells were lysed, and luciferase activity was quantified. (D) Primary hepatocytes of IFNAR1-deficient and wild-type mice were incubated for 3 h with 25 μM TCDC before infection with Δm157-MCMV-luciferase (0.1 PFU/cell). At 24 h postinfection, the cells were lysed and the luciferase activity was quantified.