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BK polyomavirus (BKV) is a ubiquitous pathogen that establishes lifelong latency in the renal tubular epithelium and urothelium, often reactivating in immunocompromised individuals such as transplant recipients (Hirsch & Randhawa, 2019, ASID). The BKV VP1 peptide-MHC complex represents the presentation of the virus's major capsid protein (VP1) fragments on the surface of infected cells via Major Histocompatibility Complex (MHC) molecules (UniProt P03088). This complex is the critical ligand for the T-cell receptor (TCR) of BKV-specific CD8+ cytotoxic T lymphocytes, which are essential for controlling viral replication (Babel et al., 2011, American Journal of Transplantation). In clinical settings, BKV reactivation can lead to BKV-associated nephropathy (BKVAN) in kidney transplant patients or hemorrhagic cystitis in hematopoietic stem cell transplant recipients. Therapeutic interventions targeting these complexes include adoptive T-cell therapies, such as posoleucel (ALVR106), which utilize donor-derived T cells to recognize and eliminate cells displaying these viral antigens (AlloVir, 2023; NCT04354831). Monitoring BKV viral load and the presence of specific HLA alleles are common practices for managing patients at risk of BKV-related complications.
T-cell receptor (TCR) mediated recognition and subsequent cytotoxic lysis of infected cells.
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