Fig. 5: Clinical isolates of PeV-A1 (52967 and 51067) and PeV-A3 (178608 and 51903) showed infection and replication in UNOs and PeV-A3 initiated a succeeding inflammatory response.

a Relative increase in viral RNA copies in the supernatant at 0, 5, and 10 dpi normalized to 0 dpi. b Infectious viral particles in supernatant at 0, 5, and 10 dpi. c Venn diagram representing DAPs upon infection in organoids with clinical isolates of PeV-A1 and PeV-A3 or E11 compared to mock infection samples. d Bubble plot represents −log10 scaled adjusted P value (adjusted P value < 0.1, Piano) enrichment of corresponding upregulated (green) or downregulated (yellow) pathways upon infection. e Venn diagram representing the number of overlapping pathways up or downregulated upon infection (adjusted P value < 0.1, Piano). f Significantly altered IFN-related proteins due to infection with clinical isolates of PeV-A compared to MOCK, presented in boxplots, *P value < 0.05; **P value < 0.01 obtained in Limma. Quantile normalized protein abundance values are shown in the Y axis. The boxes represent the interquartile range and the whiskers represent minimum and maximum values. a, b In all cases, data correspond to the geometric mean ± geometric standard deviation (SD) of four technical replicates of three batches of UNOs. Statistical significance was analyzed per virus using a Kruskal–Wallis test with multiple comparisons, *P value < 0.05; **P value < 0.01; ***P value < 0.001; ****P value < 0.0001. c–f Data correspond to two technical replicates (individual organoids) in three batches (independent experiments) of organoids. DAPs are differentially abundant proteins. Source data are provided as a Source Data file.