Early IFNAR inhibition promotes transitional T _PEX cell formation prior to establishing the T _SCM cell population. (A–H) scRNAseq analysis of 17629 P14 cells from peripheral lymph nodes at d8 acute LCMV, d8 chronic LCMV, and d8 and d14 IFNAR-blocked acute LCMV infection conditions. Data show three to four biological replicates per condition. (A and B) UMAPs of CD8⁺ T cells (A) based on infection condition and (B) prominence of each condition per cluster. (C) Module scores of T_SCM-, T_PEX-, and T_EX-associated genes in prominent populations from each condition. (D) Normalized mean expression heat map of classed marker genes in selected clusters, normalized as z-scored log counts across conditions. (E and F) NES plots of enrichment of (E) T_PEX cell, exhausted progenitor (T_PROG) cell, and T_EX cell gene programs from published datasets, and (F) enrichment of hallmark Wnt signaling and stemness signatures. (G) Venn diagram reflecting distinct and intersecting GEX in selected clusters. (H) MA plot of log fold change versus mean expression between C2 (comprising cells from chronic LCMV and d8 IFNAR-blocked acute LCMV) and C0+C8 (comprising cells from d14 IFNAR-blocked acute LCMV and control acute LCMV). Marked genes represent intersections of the Venn diagram in G, genes shared by each cluster (green), genes shared in C2 (orange), genes shared in C0+C8 (purple). DE genes identified in G came from analysis using the voom-limma pipeline with duplication correlation and P <0.05. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Fig. S2 shows additional supporting data. HSC-LT, long-term hematopoietic stem cells. YF, Yellow Fever.