LCMV Cl13 infection induces dysregulation in tight junction gene expression as well as a type I IFN signature in IECs. See also Fig. S3, Table S1, Table S2, Table S3, Table S4, and Table S5.C57BL/6 mice were infected with LCMV ARM or Cl13 or left uninfected (Un) and RNA-sequencing analysis was performed on FACS-purified IECs on day 9 p.i. (A) Number of DEGs with adjusted P value (p.adj) < 0.05 and fold change (FC) ≥ 2 between IECs from ARM- or Cl13-infected versus uninfected mice. (B) PCA plot with IEC transcriptomes from uninfected and ARM- and Cl13-infected mice. PC, principal component. (C) Gene counts by DESeq2 for indicated genes were normalized to average counts in the uninfected group. (D) Differentially enriched pathways (P < 0.05; FDR < 0.25) in ARM- versus Cl13-infected mice by GSEA. (E) DEGs in ARM- versus Cl13-infected mice. RNA sequencing was performed in a total of three independent experiments, in which each sequenced sample consists of IECs pooled from three mice. Averages ± SEM are shown (C). DEG (A and E), PCA (B), and FDR-adjusted P values (C) were computed by DESeq2. *, adjusted P value < 0.05.