Fig. 4

Influenza virus stimulates cGAS- and STING-dependent IFN-β gene expression in mouse lung fibroblast. a, b Primary lung fibroblast prepared from WT, cGAS-, STING-, and MAVS-deficient mice were infected with WT PR8 (a) or ΔNS1 influenza virus (b). IFN-β mRNA levels were assessed by quantitative PCR with GAPDH as an internal control. c Samples from HEK293FT cells stably expressing EGFP (EGFP-293FT) or cGAS (cGAS-293FT) were infected with PR8 or EMCV. Cell lysates were collected at 9 h post infection and blotted using the indicated antibodies. d EGFP-293FT or cGAS-293FT cells were infected with influenza virus (left panel) or EMCV (right panel) for 24 h. IFN-β mRNA levels were assessed by quantitative PCR with β-actin as an internal control. e, f STING-A549 cells (e) or lung fibroblasts (f) were infected with PR8 virus. Pure cytosolic extracts were collected at indicated time points and analyzed for cGAMP by ELISA. These data are from three independent experiments (a, b, d–f; mean ± s.e.m.). *P < 0.05, **P < 0.01, ***P < 0.001; (one-way ANOVA and Tukey’s test). Source data are provided as a Source Data file