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. | Nature Microbiology

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

Fig. 2

a, Schematics of YFV genome organization. bd, 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.

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