Figure 7. In the absence of STING, the impairment of MCMV m152stop in vivo is rescued.

• A–C
  Type I IFN levels in spleen homogenates (A) and serum (B) and IL‐6 levels in spleen homogenates (C) of C57BL/6J (B6J) or STING^−/− mice following i.v. infection with 4 × 10⁵ PFU parental MCMV or MCMV m152stop were analyzed 6 hpi by ELISA. IFNβ levels of STING^−/− mice were below the detection limit (n.d.).
• D
  B6J or STING^−/− mice were i.v. infected with 4 × 10⁵ PFU parental MCMV or MCMV m152stop. Six hpi, RNA was extracted from spleen homogenates and expression of MCMV IE1 and E1 transcripts was determined by qRT–PCR.
• E
  B6J or STING^−/− mice were i.v. infected with 4 × 10⁵ PFU parental MCMV. Six hpi, RNA was extracted from spleen homogenates and m152 transcript levels were determined by qRT–PCR.
• F
  B6J or STING^−/− mice were depleted of NK cells via treatment with anti‐NK1.1 (right panel) or left untreated (left panel). One day after NK cell depletion, B6J or STING^−/− mice were i.v. infected with 4 × 10⁵ PFU parental MCMV or MCMV m152stop. Sixteen hpi, RNA was extracted from spleen homogenates and MCMV E1 transcript levels were determined by qRT–PCR. Data were normalized to 10⁷ cellular β‐actin transcripts (D–F).

Data information: n = 5–6 mice per group; Student's t‐test (unpaired, two‐tailed), n.s. not significant, **P < 0.01, ***P < 0.001, ****P < 0.0001.