Extended Data Fig. 7: Enhanced cerebral pathogenesis of HSE in Shisa9-/- mice.
From: Modulation of virus-induced neuroinflammation by the autophagy receptor SHISA9 in mice
(a) Survival curve of wild-type (WT) and Shisa9−/− mice (n = 14 per group) post HSV-1 infection; P-values were determined by the log-rank test. (b) HSV-1 yield in WT and Shisa9−/− mice post HSV-1 infection. (c) WT and Shisa9−/− Mice (n = 9 per group) were intracranial infected with HSV-1 (1 × 102 PFU), scored for neuroinflammation symptoms. Data are presented as mean ± SD of 9 mice. Similar results were obtained by three independent experiments. Stars refers to difference between WT and Shisa9−/− for total 9 days. (d) ELISA of indicated cytokines in brain homogenates in WT and Ikbke−/− mice at 12 days after intracranial infection with HSV-1 (1 × 102 PFU). All error bars, mean ± SD of 12 mice. (e) Representative image (left) and quantification (right) of histology of WT and Shisa9−/− mice brain. Scale bars, 200 μm (main panels), and 50 μm (right panel, enlarged view). Data are presented as mean ± SD of 6 mice. (f-h) WT and Shisa9−/− mice were intracranial infected with VSV (1 × 102 PFU) (f) Survival of wild-type (WT) and Shisa9−/− mice (n = 32 per group) at various times (horizontal axis), P-values were determined by the log-rank test. (g) ELISA of indicated cytokines in brain homogenates were detected 12 days post infection. (h) VSV-G staining and H&E staining of hippocampi area. Scale bars, 200 μm. Data are presented as mean ± SD of 12 mice in (g) and mean ± SD of 9 mice in (h). (i) Real-time quantitative polymerase chain reaction (qPCR) analysis of brain homogenates of WT and Shisa9−/− mice (12 days after inoculated with a combination of HSV-1 (2 × 102 PFU) and lysosome inhibitor Lys05 (16 mg/kg)). Data are presented as mean ± SD of 6 mice. For (b, d, e, g-i), P-values were determined by unpaired two-tailed Student’s t test, for (c), by Two-way ANOVA.
