Fig. 2: A KD-specific 13 transcript signature³⁷ shows that KD and MIS-C are indistinguishable, but ViP/sViP signatures place MIS-C as farther along the spectrum than KD.

a Schematic displays the workflow for patient blood collection and analysis by RNA Seq (this figure) and cytokine array by mesoscale (Figs. 4 and 5). b, c Bar (top) and violin (bottom) plots display the classification of blood samples that were collected during collected during acute (AV) and sub-acute (SA; ~10–14 days post-discharge) visits of KD subjects and from patients diagnosed with MIS-C. The p value for comparison between acute KD (AV) and MIS-C (M) is displayed in red font. d, e Heatmaps display the patterns of expression of the 166 genes in ViP (d) and 20 gene sViP (e) signatures in the KD and MIS-C samples. The only cytokine–receptor pair within the signature, i.e., IL15/IL15RA, are highlighted on the left in red font in (d). f Schematic displays the 13-transcript whole blood signature (no overlaps with ViP signature genes) previously demonstrated to distinguish KD from other childhood febrile illnesses³⁷. g and h Bar (top) and violin (bottom) plots display the classification of blood samples that were collected during acute (AV) and convalescent (CV) visits from two independent KD cohorts (g; Historic Cohort 1; e; Prospective Cohort 2) using 13-transcript KD signature. FC, febrile control. See also Supplementary Fig. S1 for co-dependence analysis of ViP and KD-13 signatures. Welch’s two sample unpaired two-sided t-test is performed on the composite gene signature score to compute the p values. In multi-group setting each group is compared to the first control group and only significant p values are displayed. The p value for comparison between acute KD (AV) and MIS-C (M) is displayed in red font.