Figure 5: Dissemination of the IFN response in the infected brain depends on STING.

(a) Tissue sections from the brain stem of WT and Sting^gt/gt mice infected for 6 days with HSV-1 (1 × 10⁶ PFU per eye) were stained with an antibody against viperin, HSV-1 and Iba1 (microglia), n=4–6 mice per group. Scale bar, 20 μm. Boxed cells are magnified in the images to the left and right of the large images. (b–d) Astrocytes, neurons and microglia from WT and Sting^gt/gt mice were cultured in vitro, treated with IFN-α/β (25 U ml⁻¹) and infected with HSV-1 (MOI 1). Supernatants were isolated 48 h later, and virus yield was measured by plaque assay. Data are presented as means ± s.e.m., n=5–8. (e,f) Neurons and astrocytes were cultured in vitro and treated with IFN-α/β (25 U ml⁻¹) and infected with HSV-1 (MOI 1). Total RNA was isolated 6 h later and analysed for IFN-β mRNA levels. Data are normalized to β-actin levels and are presented as (means ± s.e.m.) fold induction relative to the WT UT, n=5–8 per group Symbols for P-values used in the figures: *0.01<P<0.05; **0.001<P<0.01; ***P<0.001; NS, not significant.