BK polyomavirus VP2 capsid protein-derived peptide-HLA class I complex (BKV VP2-HLA-I)

BK polyomavirus (BKV) is a double-stranded DNA virus that establishes lifelong latency in the renal tubular epithelium and urothelium (Hirsch HH, et al., 2019, PMID: 30811824). In immunocompromised individuals, particularly kidney transplant recipients, BKV can reactivate, leading to BKV-associated nephropathy (BKVAN) and potential graft failure (Shingadia D, et al., 2020, PMID: 32166531). The VP2 protein is a minor structural component of the viral capsid that is expressed during the late phase of the viral life cycle and is essential for viral entry (UniProt, P03089). Peptides derived from the VP2 protein are processed and presented on the cell surface by Human Leukocyte Antigen (HLA) class I molecules, serving as critical targets for CD8+ cytotoxic T lymphocytes (Leboeuf C, et al., 2017, PMID: 28630092). Therapeutic strategies targeting these peptide-HLA complexes include the infusion of virus-specific T cells (VSTs), such as Posoleucel, or the development of TCR-engineered T cells designed to recognize and eliminate BKV-infected cells (Olson A, et al., 2021, PMID: 33548344). Monitoring BKV viral load and the presence of VP2-specific T cells are essential for managing infection and evaluating the efficacy of these immunotherapies in clinical settings.

Other names

BKV VP2 peptide-MHC complexBK virus VP2 antigenBKV VP2-HLA complexBK polyomavirus minor capsid protein VP2BKV VP2-derived epitopes

T-cell receptor (TCR) mediated recognition of the peptide-HLA complex leading to cytotoxic T-lymphocyte activation and lysis of infected cells.