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. 2023 Mar 13;3(4):418–435. doi: 10.1038/s43587-023-00379-0

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a, Summary of mutation counts and synthesized and validated epitopes from 13 SARS-CoV-2 variant strains. b,c, Comparison of ancestral and mutant epitope binding affinity to HLA-A2 on T2 cells. Ancestral and mutant epitopes are listed in black and red, respectively, in b. Paired ancestral and mutant epitopes are listed adjacently. Numeric superscripts in b correspond to ID numbers in a. Blank, no peptides; NC, negative control, EBV virus peptide IVTDFSVIK; PC, positive control, influenza A M1 peptide GILGFVFTL. The same applies throughout the paper. d, Evaluation of ancestral and mutant SARS-CoV-2 epitope binding to HLA-A2 by ELISA assay. Data are shown as mean ± s.d., n = 3 independent experiments for each tested epitope. ****P < 0.0001 (two-sided t-test, comparing to NC). Threshold for peptide MHC (pMHC) formation positivity was set as above the average OD value of the negative control. HLA: control UV-sensitive peptide without UV irradiation.