FigureĀ 5.
EBV genome variation in intervals encoding prototypic T-cell epitopes is predicted to generate variant peptides with altered binding to class I MHC molecules. (A) Heat map of predicted binding affinity (BA) of 30 prototypic EBV- encoded CD8+ T-cell epitopes (rows) to 16 class I MHC alleles (columns) and of the corresponding peptides encoded by EBV genome variants. The far-right column contains a heat map of the frequency of the EBV genome variant that encodes each peptide in the 1376 EBV genomes meeting predetermined quality metrics in this study. (B) Heat map indicating the presence (blue) or absence (white) of the class I MHC alleles known to present 6 prototypic EBV-encoded peptides to CD8+ T cells in the 50 most frequent class I MHC haplotypes in Guatemala (left) and China (right). The associated class I MHC allele is shown in bold beneath each peptide. NB, no binding; SB, strong binder; WB, weak binder.

EBV genome variation in intervals encoding prototypic T-cell epitopes is predicted to generate variant peptides with altered binding to class I MHC molecules. (A) Heat map of predicted binding affinity (BA) of 30 prototypic EBV- encoded CD8+ T-cell epitopes (rows) to 16 class I MHC alleles (columns) and of the corresponding peptides encoded by EBV genome variants. The far-right column contains a heat map of the frequency of the EBV genome variant that encodes each peptide in the 1376 EBV genomes meeting predetermined quality metrics in this study. (B) Heat map indicating the presence (blue) or absence (white) of the class I MHC alleles known to present 6 prototypic EBV-encoded peptides to CD8+ T cells in the 50 most frequent class I MHC haplotypes in Guatemala (left) and China (right). The associated class I MHC allele is shown in bold beneath each peptide. NB, no binding; SB, strong binder; WB, weak binder.

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