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Epstein-Barr virus (EBV) peptide–Human Leukocyte Antigen (HLA) complexes are molecular structures formed when viral peptides are processed and presented on the surface of infected cells by HLA molecules. These complexes serve as the primary recognition signal for the cellular immune system, specifically for CD8+ cytotoxic T cells and CD4+ helper T cells (Source: PubMed, PMID: 31435312). In EBV-associated malignancies and post-transplant lymphoproliferative disorders (PTLD), these complexes are critical targets for adoptive T-cell therapies and vaccines (Source: EMA, Ebvallo Assessment Report). Therapeutic strategies involve using EBV-specific T cells or engineered T-cell receptor (TCR) therapies that bind specifically to these peptide-HLA combinations to induce apoptosis in infected or malignant cells. Because EBV persists latently in B cells, the presentation of these peptides is essential for maintaining viral latency and preventing uncontrolled B-cell proliferation (Source: Nature Reviews Immunology, doi:10.1038/nri.2016.107). The specificity of these interactions is determined by the specific EBV epitope and the patient's HLA genotype, making HLA typing a prerequisite for many of these therapies (Source: Blood, doi:10.1182/blood.2020009295).
Targeted recognition by T-cell receptors (TCRs) on cytotoxic T lymphocytes or engineered T-cells, leading to the lysis of EBV-infected cells.
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