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BK virus antigen-derived peptides presented on Human Leukocyte Antigen (HLA) molecules serve as the primary recognition signal for the cellular immune system to identify and eliminate BK polyomavirus (BKV) infected cells (Source: PubMed, PMID: 31209018). These complexes consist of short viral protein fragments, typically derived from the Large T-antigen or capsid proteins like VP1, bound within the groove of HLA Class I or Class II molecules (Source: UniProt). In immunocompromised individuals, such as kidney or hematopoietic stem cell transplant recipients, the failure of the immune system to recognize these targets leads to BKV reactivation. This reactivation can result in severe clinical conditions, including BK virus-associated nephropathy (BKVAN) or hemorrhagic cystitis (Source: NIH, StatPearls). Therapeutic strategies targeting these complexes include the adoptive transfer of donor-derived or "off-the-shelf" BKV-specific T cells (VSTs), such as Posoleucel (Source: AlloVir). These therapies aim to restore the host's ability to target BKV-infected cells specifically, thereby reducing viral load and preventing organ damage. Monitoring BKV-specific T-cell responses and viral load serves as a critical biomarker for assessing the efficacy of these interventions (Source: Journal of Clinical Investigation). The specificity of the TCR for the peptide-HLA complex is crucial to avoid off-target effects or graft-versus-host disease.
T-cell receptor (TCR) mediated recognition of BKV peptides presented on HLA, triggering cytotoxic T-lymphocyte (CTL) activation and lysis of infected host cells.
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