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Cytomegalovirus (CMV)-derived peptides presented by HLA class I molecules are essential targets for the cellular immune system to control Human Cytomegalovirus (HCMV) infection [1]. These peptides are generated through the proteasomal degradation of viral proteins—including well-known antigens like pp65 and IE1, as well as other less dominant proteins like pp150, gB, or IE2—and are subsequently loaded onto HLA class I molecules for surface display [2]. CD8+ cytotoxic T cells recognize these specific peptide-HLA complexes via their T-cell receptors (TCRs), leading to the lysis of infected cells and the secretion of antiviral cytokines [1]. In therapeutic contexts, these complexes are utilized in the development of peptide-based vaccines and adoptive T-cell transfer (ACT) protocols, particularly for immunocompromised patients such as transplant recipients who are at high risk for CMV reactivation [3]. Targeting a broad range of CMV peptides, including those beyond the immunodominant ones, helps overcome viral immune evasion strategies and ensures a more robust, polyfunctional T-cell response [2]. Sources: [1] Walker et al. (2007) Reviews in Medical Virology; [2] Sylwester et al. (2005) Journal of Experimental Medicine; [3] Riddell & Greenberg (1995) Annual Review of Immunology.
Induction or restoration of antigen-specific CD8+ T-cell immunity by providing targets for T-cell receptor (TCR) recognition on infected cells.
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