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Epstein-Barr virus (EBV) derived peptides presented by HLA class I molecules are fragments of EBV proteins processed by infected cells and displayed on the cell surface via HLA class I (also termed MHC class I) molecules[1][2][4]. These peptide-MHC complexes enable the immune system, particularly CD8⁺ cytotoxic T lymphocytes, to recognize and selectively destroy EBV-infected cells[4]. The spectrum of presented peptides includes both immunodominant epitopes from latent and lytic EBV proteins, such as EBNA3A/3B/3C, LMP1, and LMP2A, which vary in their presentation depending on the HLA allele present in the individual host[1][7]. These complexes are central both to the normal immune clearance of EBV infection and to the surveillance for EBV-driven malignancies (e.g., Hodgkin lymphoma, nasopharyngeal carcinoma); loss or alteration of peptide presentation by HLA class I is a well-described mechanism of immune evasion by the virus[1][2][4]. Therapeutic approaches—including adoptive cell therapies, vaccines, and TCR-like antibodies—aim to restore or harness recognition of these complexes on infected or malignant cells[2][4].
T cell receptor (TCR) or antibody binding triggers cytotoxic T cell or immune effector cell responses against EBV-infected cells presenting viral peptides[2][4]. Therapeutic interventions may aim to boost presentation or recognition of these peptides to enhance immune clearance of EBV-infected or malignant cells[2].
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