Fig. 2

In WT and Rag1^−/− mice but not Ifnar1^−/− mice, ZIKV is restricted to the CNS following intracranial infection. a Following i.c. infection, ZIKV RNA is detectable in the CNS of WT (black), Ifnar1^−/− (red) and Rag1^−/− mice (blue). However, ZIKV RNA is only detectable in the livers and testes of Ifnar1^−/− mice but not WT or Rag1^−/− mice. *p < 0.05 when compared with the corresponding time point in WT mice, ^p < 0.05 when compared with the corresponding time point in Ifnar1^−/− and Rag1^−/− mice, and #p < 0.05 compared to sham-injected mice as determined by one-way ANOVA with Tukey’s multiple comparisons test. b In situ hybridization shows that at peak disease, ZIKV predominantly infects the cortex, hippocampus, and thalamus of i.c.-infected WT mice. At peak disease, in Ifnar1^−/− and Rag1^−/− mice, the virus spread to the brain stem and in Ifnar1^−/− mice, ZIKV also infects the cerebellum. c Dual-label immunofluorescence (DL-IF) was performed with antibodies against flavivirus NS1 and markers to detect neurons (NeuN), astrocytes (GFAP), or microglia (Iba1). DAPI was used to stain nuclei. Co-localization of ZIKV NS1 protein and cell type marker is evident by orange/yellow color. DL-IF shows that ZIKV infects predominantly neurons but not astrocytes or microglia independent of the genotype. Representative images of a WT, Ifnar1^−/−, and Rag1^−/− hippocampus are shown