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Cytomegalovirus (CMV) peptide antigens presented on Human Leukocyte Antigen (HLA) molecules are the primary targets for the adaptive cellular immune response against CMV infection. These complexes consist of short viral peptide fragments, most commonly derived from immunodominant proteins like pp65 (UL83) or IE1 (UL123), bound within the groove of HLA Class I or Class II molecules on the surface of infected cells (UniProt, PubMed). The recognition of these peptide-MHC (pMHC) complexes by the T-cell receptors (TCRs) of CD8+ cytotoxic T cells and CD4+ helper T cells is essential for the control of viral latency and reactivation (NIH, PubMed). In therapeutic contexts, these complexes are targeted by adoptive T-cell therapies, such as virus-specific T cells (VSTs), and various vaccine candidates designed to elicit a robust T-cell response (AlloVir, ClinicalTrials.gov). Because CMV is a major cause of morbidity in immunocompromised individuals, such as hematopoietic stem cell or solid organ transplant recipients, targeting these pMHC complexes is a key strategy for preventing and treating CMV-related diseases (PubMed). The specificity of these interactions is strictly governed by the patient's HLA genotype, making HLA matching a critical factor in the efficacy and safety of pMHC-targeted therapies (PubMed).
Recognition by T-cell receptors (TCRs) on CD8+ or CD4+ T cells, leading to the lysis of infected cells or secretion of antiviral cytokines.
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