Figure 2. STING is required for effective in vivo host defence.

a, Sting-deficient animals (Sting^−/−) or littermate controls (Sting^+/+) (n = 7; approximately 8-weeks-of-age) were infected with HSV-1 (1 × 10⁷ i.v.) and survival was monitored. b, Sting^−/− or control mice were infected with HSV-1 as in a and brains were retrieved after 5 days for HSV-1 plaque assays. p.f.u., plaque-forming units. c, d, Serum from animals (n = 3) infected with HSV-1 (1 × 10⁷ i.v.) was analysed for IFNβ (c) or IFNα (b) production after 6 h. e, f, Serum from animals infected as in c was analysed for RANTES (e) and IL6 (f) production. g, Sting^−/− or control mice (n = 6) were infected with VSV (5 × 10⁷ i.v.) and survival was monitored. h, i, Mice (n = 3) were treated as in g and IFNβ (h) or IFNα (i) was measured after 6 h. j, Increasing amounts of YFV NS4B were co-transfected into 293T cells with human STING or the amino terminus of RIG-I (ΔRIG-I, residues 1–284) and transfected IFNβ promoter-driven luciferase (IFNβ-Luc) was measured after 36 h. k, Immortalized MEFs were transfected with YFV NS4B for 24 h, infected with VSVΔM⁴ (m.o.i. 1) for 16 h, and IFNβ was measured. l, 293 cells were transfected with NS4B–HA for 36 h and after immunoprecipitation (IP) with anti-haemagglutinin antibody, were analysed by western blot (WB) using anti-STING serum. *P < 0.05, Student's t-test. Error bars indicate s.d.