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Pathogen-derived peptide–HLA complexes from varicella–zoster virus (VZV) are critical molecular targets for the adaptive immune system, consisting of viral protein fragments presented on the surface of infected cells by Human Leukocyte Antigen (HLA) molecules (Source: PubMed, PMID: 31209227). These complexes are primarily recognized by T-cell receptors (TCRs) on CD8+ cytotoxic T cells and CD4+ helper T cells, which are essential for controlling primary VZV infection (chickenpox) and preventing the reactivation of the latent virus as herpes zoster (shingles) (Source: Journal of Virology, doi:10.1128/JVI.01710-16). Major viral antigens involved in these complexes include glycoprotein E (gE) and immediate-early proteins like IE62, which are frequently targeted by current vaccines such as Shingrix (Source: NIH, National Institute of Allergy and Infectious Diseases). In a therapeutic context, these pMHC complexes serve as the basis for developing highly specific TCR-engineered T-cell therapies and diagnostic tools to monitor VZV-specific immune competence in immunocompromised patients (Source: Nature Communications, doi:10.1038/s41467-020-14819-w). Understanding the structural biology of these complexes is vital for designing next-generation immunotherapies that can bypass viral evasion mechanisms and provide long-lasting protection against postherpetic neuralgia (Source: Frontiers in Immunology, doi:10.3389/fimmu.2018.01846).
Recognition of the peptide-HLA complex by specific T-cell receptors (TCRs) on CD4+ or CD8+ T cells, leading to immune activation and clearance of virus-infected cells.
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