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BK polyomavirus (BKV) is a double-stranded DNA virus that remains latent in the urinary tract of most healthy individuals but can reactivate under conditions of profound immunosuppression, such as those following kidney or hematopoietic stem cell transplantation. The VP1 protein is the primary structural component of the BKV capsid and serves as a major target for the host's cellular immune response (Pinto et al., 2013, PMID: 23613444). During viral replication, VP1-derived peptides are processed and presented on the surface of infected cells by Major Histocompatibility Complex (MHC) class I molecules. These peptide-MHC complexes are specifically recognized by the T-cell receptors (TCRs) of CD8+ cytotoxic T lymphocytes, which then mediate the destruction of the infected cells and control viral spread (Li et al., 2006, PMID: 16415004). Therapeutic strategies targeting these complexes include the infusion of ex vivo expanded BKV-specific T cells (VSTs) or the development of TCR-engineered T-cell therapies, such as Posoleucel, to treat BKV-associated nephropathy and hemorrhagic cystitis (Blyth et al., 2013, PMID: 23297125). The efficacy of these treatments is often dependent on the patient's HLA type, with certain epitopes like the HLA-A*02:01-restricted VP1 p108 peptide being highly immunodominant.
T-cell receptor-mediated recognition of viral epitopes presented on MHC class I, leading to the activation of cytotoxic T lymphocytes and subsequent lysis of infected host cells.
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