STING is required for host defense against neuropathological West Nile virus infection
Fig 2
STING is not required for viral control of WNV in neurons in vitro or in the CNS during intracranial infection in vivo.
(A) WNV viral load in macro-dissected brain sections (cortex, sub-cortex, cerebellum and brain-stem) and spinal cord of WT and STING-/- infected mice, D4 and D8 post infection. n = 6–10 per strain per time-point. Graphed as stacking points. Limit of detection indicated by dashed line. Unpaired students t-test; p = 0.05*; p = 0.005**. (B) WNV IHC in the brains of mock infected and WNV infected WT and STING-/- Terminal and Survivor cohort. Mock tissues are unremarkable with non-specific staining of capillaries (arrows). Terminal mice have punctate staining near foci of gliosis (WT, circle) or neuronal degeneration (WT and STING-/-, arrows). No discernable specific signal for WNV antigen was observed in either WT or STING-/- Survivors, despite observable gliosis in STING-/- (circle). All panels, original magnification 200X. (C) TUNEL IHC stains of representative WT and STING-/- Survivor (18 dpi) mice. Brown stain indicates neuronal death. (D). Single and multistep virologic analysis of primary cortical neurons from WT and STING-/- mice. Pooled samples of 3 embryos per genotype. (E) Titer in mice infected with WNV via intracranial inoculation D4 pi. n = 6 WT and n = 5–6 STING-/-. Students t-test, p = 0.05*; p = 0.005**.