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BK polyomavirus (BKV) peptide antigens presented on MHC class I molecules are the primary targets for the host's cytotoxic T-cell response. These complexes consist of short viral peptide fragments, typically derived from the Large T-antigen or capsid proteins like VP1, which are processed and displayed on the surface of infected cells within the groove of Major Histocompatibility Complex (MHC) class I molecules. In healthy individuals, these targets allow the immune system to maintain BKV in a latent state; however, in immunocompromised patients, such as kidney or bone marrow transplant recipients, the failure of T-cell recognition leads to viral reactivation. This reactivation can cause severe conditions like BK polyomavirus-associated nephropathy (BKVAN) and hemorrhagic cystitis. Therapeutic interventions, such as adoptive virus-specific T-cell (VST) therapies, specifically target these MHC-peptide complexes to restore immune control and eliminate infected cells.
Recognition of the peptide-MHC complex by the T-cell receptor (TCR) of CD8+ cytotoxic T lymphocytes, triggering the release of perforin and granzymes to induce apoptosis in the infected cell and the secretion of antiviral cytokines like IFN-gamma.
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