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Human polyomavirus 2 (HPyV-2), commonly referred to as the JC virus (JCV), is a double-stranded DNA virus that remains latent in the majority of the human population. In individuals with compromised immune systems, the virus can reactivate and infect oligodendrocytes and astrocytes in the brain, leading to progressive multifocal leukoencephalopathy (PML) [1]. The target consists of viral peptide antigens, primarily derived from the Large T-antigen and the VP1 capsid protein, which are presented on the surface of infected cells by Major Histocompatibility Complex (MHC) class I molecules [2]. These peptide-MHC complexes are the essential ligands for CD8+ cytotoxic T lymphocytes (CTLs), which recognize and destroy the infected cells to control the infection. Therapeutic interventions targeting these antigens include adoptive transfer of virus-specific T cells (VSTs) and the development of TCR-engineered T cells designed to enhance the cellular immune response against JCV [3]. Monitoring the presence and frequency of T cells specific to these HPyV-2 antigens is a critical biomarker for predicting clinical outcomes in PML patients [4].
T-cell receptor (TCR) mediated recognition and cytotoxic lysis of infected cells
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