BK virus VP1 capsid protein-derived peptides presented on MHC (BKV VP1-MHC)

BK virus VP1 capsid protein-derived peptides presented on MHC represent a critical target for cellular immunotherapy in immunocompromised patients, particularly those undergoing hematopoietic stem cell or solid organ transplantation (Leboeuf et al., 2017, American Journal of Transplantation). The VP1 protein is the primary structural component of the BK polyomavirus (BKV), and its degradation products are processed and displayed on the surface of infected cells by Major Histocompatibility Complex (MHC) molecules, such as HLA-A*02:01 (UniProt P03088). Recognition of these peptide-MHC complexes by the T-cell receptors (TCRs) of CD8+ cytotoxic T lymphocytes triggers the elimination of virus-infected cells (Papadopoulou et al., 2014, Science Translational Medicine). In the context of BK virus-associated nephropathy (BKVAN) or hemorrhagic cystitis, where the virus reactivates due to immunosuppression, therapeutic strategies such as adoptive transfer of virus-specific T cells (VSTs) like Posoleucel (ALVR106) are employed to restore viral control (AlloVir, 2023). These therapies specifically bind to the VP1-MHC complex to induce targeted cell lysis and reduce viral load, providing a precision approach to managing polyomavirus-related complications (Blyth et al., 2013, Blood). This target is unique because it is not a single molecule but a molecular complex that serves as a signature for virally infected cells, allowing the immune system to distinguish them from healthy tissue.

Other names

BKV VP1 antigen-MHC complexHLA-presented BK virus VP1 peptidesBK polyomavirus VP1-HLA complexBKV VP1 epitopes

T-cell receptor (TCR) mediated recognition of the peptide-MHC complex leads to the activation of cytotoxic T lymphocytes, which subsequently release perforins and granzymes to induce apoptosis in BK virus-infected cells (Papadopoulou et al., 2014, Science Translational Medicine).