Figure 1: Mice deficient in cGAS or STING are susceptible to HSE and exhibit impaired antiviral responses.

Mice were infected in the cornea with 1 × 10⁶ PFU per eye of HSV-1 (strain Mckrae). On subsequent days, animals were scored for (a) eye swelling, (b) hydrocephalus, and (c) symptoms related to neurological disease and (d) survival. (e) Route of virus spread from the eye to the CNS. (f–i) Eye washes, trigeminal ganglia, brain stem and brains were isolated on the indicated time points post infection, and viral load was quantified using plaque assay. n=9 mice per group (a–i). (j) Tissue section from the brain stem of WT and Sting^gt/gt mice infected for 6 days with HSV-1 were stained with anti-HSV-1. n=5-6 mice per group. The original magnifications are 2.5 × and 20 × for the zoomed in images. (k–l) The number of HSV-1-positive cells in six tissue sections from the medulla and pons were quantified, and presented as means ± s.e.m. n=3–9 per group. (m–o) Organotypic brain slices from WT and Sting^gt/gt mice were cultured and infected with 5 × 10³ PFU of HSV-1. The viral load in (n) the culture medium on day 2 and (o) in homogenized brain slices on 6 days post infection was determined by plaque assay. Data are shown as mean values ± s.e.m., n=6–8 wells with three brain slices in each. Symbols for P-values used in the figures: *0.01<P<0.05; **0.001<P<0.01; ***P<0.001; NS, not significant. Red and green asterisks indicate P-values between WT and relevant KO mice at specific days post infection.