BK virus and JC virus peptide antigens presented on HLA class I and II (BKV/JCV pMHC)

BK virus (BKV) and JC virus (JCV) are opportunistic polyomaviruses that cause significant morbidity in immunocompromised patients, particularly those undergoing hematopoietic stem cell or solid organ transplantation (NIH, 2024). The target involves viral peptide antigens, such as those from the Large T-antigen and VP1 capsid protein, which are processed and presented by Human Leukocyte Antigen (HLA) class I and II molecules on the surface of infected cells (Nelson et al., 2017; Papadopoulou et al., 2014). Due to the high degree of sequence homology between BKV and JCV, many T-cell epitopes are cross-reactive, allowing a single T-cell population to recognize and respond to both viruses (Nelson et al., 2017). Therapeutic strategies targeting these peptide-HLA complexes primarily involve adoptive cell therapies, such as virus-specific T cells (VSTs), which are expanded ex vivo to recognize these specific antigens (Papadopoulou et al., 2014; AlloVir, 2023). These therapies, including investigational agents like posoleucel, aim to restore the host's cellular immune response to control viral replication and prevent diseases like BKV-associated nephropathy and progressive multifocal leukoencephalopathy (PML) (AlloVir, 2023; NIH, 2024). By specifically targeting viral antigens, these treatments offer a precision approach to managing polyomavirus infections while minimizing the risks of graft-versus-host disease or generalized immunosuppression (Papadopoulou et al., 2014).

Other names

BK polyomavirus antigensJC polyomavirus antigensBKV/JCV peptide-MHC complexesPolyomavirus-derived T-cell epitopesBKV/JCV cross-reactive antigensPolyomavirus-associated antigens

Adoptive immunotherapy using virus-specific T cells that recognize viral peptides presented by HLA molecules on infected cells, leading to targeted cytotoxicity and viral clearance (Papadopoulou et al., 2014).