Recruitment of myeloid cells into the HSV-infected Irf3 ^R278Q/R278Q brain. (A) Multidimensional scaling (MDS) of CyTOF samples to visualize the level of similarity of immune infiltration into brain stems of WT, Irf3^R278Q/R278Q, Irf3^−/− mice on day 5 after infection. (B and C) Immune cell distribution of (B) myeloid and (C) lymphoid cells in brain stems of UI (n = 3) and WT HSV-1–infected mice (WT HSV-1, n = 6). (D) Lymphoid cell distribution in brain stems from WT, Irf3^R278Q/R278Q, and Irf3^−/− mice on day 5 after infection. (E–H) Myeloid cell distribution in brain stems from WT, Irf3^R278Q/R278Q, and Irf3^−/− mice on day 5 after infection. (B–H) Data are represented as % of live CD45⁺ cells and analyzed by two-tailed two-way ANOVA for difference of means, followed by two-tailed unpaired t test of means, error bars; SD. P values <0.05 were considered statistically significant. (I) UMAP and cluster identification of scRNAseq data. (J) Marker table used for annotation of cell types. (K) Dot plot for expression of genes encoding sensors and adaptor molecules related to innate immune sensing of HSV-1 in annotated cell types. (L) Subclustering analysis of monocytes. (M) Mapping of transcript levels for four markers used to identify MHC-II^hi MoMØ onto the monocyte subpopulations identified by scRNAseq. (N) Monocyte #1 cell number per mouse in WT and Irf3^−/− mice from scRNAseq. P values below 0.05 were considered significant, *P < 0.05, **P < 0.01, and ***P < 0.001.