BK polyomavirus and JC polyomavirus antigens presented on Human Leukocyte Antigen (HLA) molecules (BKV/JCV HLA-presented antigens)

BK polyomavirus (BKV) and JC polyomavirus (JCV) are closely related viruses that remain latent in most humans but cause severe disease in immunocompromised individuals, such as transplant recipients (1). BKV is primarily associated with BK virus-associated nephropathy (BKVAN) and hemorrhagic cystitis, while JCV is the causative agent of progressive multifocal leukoencephalopathy (PML) (2). These viruses express several proteins during their life cycle, including the Large T-antigen and capsid proteins (VP1, VP2, VP3), which are processed and presented as peptides on Human Leukocyte Antigen (HLA) molecules on the surface of infected cells (3). Because BKV and JCV share significant genomic homology, many T-cell epitopes are cross-reactive, allowing for the development of broad-spectrum immunotherapies (1). Therapeutic strategies targeting these HLA-presented antigens typically involve adoptive T-cell therapy, where virus-specific T-cells (VSTs) recognize the peptide-HLA complex via their T-cell receptors (TCRs) to induce apoptosis in infected cells (2). This approach aims to restore the cellular immune response in patients who lack sufficient endogenous T-cell activity to control viral replication (3).

Other names

BK virus antigensJC virus antigensBKV/JCV peptide-HLA complexesPolyomavirus-associated antigensBKV/JCV T-cell epitopes

Adoptive T-cell therapy involving the recognition of viral peptide-HLA complexes by T-cell receptors (TCRs), leading to the targeted lysis of infected cells.