Fig. 2: Mutations in the YFV envelope and NS2A are responsible for the faster spread and higher ISG expression observed for 17D vs virulent strains.
From: Amino acid changes in two viral proteins drive attenuation of the yellow fever 17D vaccine

a, Schematics of YFV genome organization. b–d, Phenotypic comparison of mScarlet reporter 17D, Asibi, Dakar and viral chimaeras. Frequency of mScarlet-positive cells (MOI = 0.05) (b), and relative expression of IFIT2 (c) and IFIT3 (d) (MOI = 0.5) were measured by flow cytometry (b) or RT–qPCR (c,d). Data are mean ± s.d. from 2 or 3 (17D and Asibi) experiments with 3 biological samples (n = 6 or 9) e, Heat map displaying the expression (by z-score) of the top-25 DEGs that were selected on the basis of their Padj in 17D- vs Asibi-infected cells. Z-score normalization was performed gene-by-gene (row-wise) on vst-transformed read counts across samples by subtracting the mean and dividing by the standard deviation. Genes were split into 4 clusters as indicated by the row breaks. f, Heat map showing sample-to-sample similarities with hierarchical clustering based on Spearman’s correlation coefficients (rs), calculated from vst-transformed data averaged across experimental replicates (n = 3 or 4) of all DEGs. Asibi or Dakar-[17D-Ens], 17D E segment with only non-synonymous mutations compared to Asibi; 17D-[Asibi-Ens], Asibi E segment with only non-synonymous mutations compared to 17D. All other chimaeras include both synonymous and non-synonymous mutations in the indicated genomic areas.