Fig. 1: SARS-Cov-2 infected K18-hACE2 mice display virus spread in the brain with extensive microglial activation and NLRP3 inflammasome upregulation.
From: SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike protein
Schematic representation for viral infection in (A). Percentage weight loss up to 12 days post infection (n=6 per group) in (B). Clinical score up to 12 days post SARS-CoV-2 infection (n = 6 per group) in (C). Representative SARS-CoV-2 infected brain at 6 dpi showing microglia marker Iba-1 (in green) and SARS-CoV-2 nucleocapsid (in red) and cell nuclei (in blue) assessed by immunofluorescence staining (n = 4 per group) in (D). Representative uninfected and SARS-CoV-2 infected brains showing microglial marker TMEM119 (in green) and SARS-CoV-2 nucleocapsid (in red) and cell nuclei (in blue) in (E). Representative uninfected and SARS-CoV-2 infected brains showing microglia marker TMEM119 (n = 4 per group) (in green) and NLRP3 (in red) and cell nuclei (in blue) in (F). Relative mRNA expression of Caspase-1 (Casp-1), Pycard (ASC) and Aif1 (Iba1) in uninfected and SARS-CoV-2 infected brains (n = 4–8 per group) in (G). Data points are means ± SEM from at least four mice per group. *P < 0.05, **P < 0.01, and ***P < 0.001 and ****P < 0.0001 by one-way analysis of variance (ANOVA) with Tukey’s post hoc test.
