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Epstein–Barr virus (EBV) peptide–Human Leukocyte Antigen (HLA) class I complexes are molecular assemblies on the surface of EBV-infected or transformed cells, consisting of viral-derived peptides bound to HLA class I molecules (Source 2.1.1). These complexes serve as the primary targets for CD8+ cytotoxic T lymphocytes (CTLs), which recognize them via their T-cell receptors (TCRs) to initiate the destruction of the target cell (Source 3.3.1). In EBV-associated malignancies like nasopharyngeal carcinoma and post-transplant lymphoproliferative disorder (PTLD), the virus expresses specific latent proteins (e.g., LMP1, LMP2, EBNA1) that are processed into peptides and presented by HLA molecules (Source 2.2.1, 3.2.3). Therapeutic strategies targeting these complexes include adoptive T-cell therapies, such as the approved drug tabelecleucel, and experimental TCR-like antibodies that mimic the specificity of T cells (Source 3.3.2, 3.4.1). A major challenge in targeting these complexes is the high polymorphism of HLA alleles, requiring therapies to be HLA-matched to the patient, and the virus's ability to downregulate HLA expression to evade immune detection (Source 2.3.1, 3.2.1).
Recognition by T-cell receptors (TCRs) or TCR-like antibodies leading to targeted cell lysis via perforin and granzyme release or antibody-dependent cellular cytotoxicity (ADCC).
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