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Varicella-Zoster Virus antigens presented by MHC molecules are short peptide fragments derived from VZV proteins (including structural and regulatory proteins), processed by infected host cells and loaded onto MHC class I and II molecules for surface display. This presentation is essential for recognition by T cells; CD8^+^ T cells monitor MHC I, while CD4^+^ T cells monitor MHC II. VZV has evolved multiple mechanisms to evade immune control, including downregulation and intracellular retention of MHC molecules—most notably through viral proteins such as ORF66 and IE4, which prevent MHC I from reaching the cell surface, thus impairing T cell recognition and killing of infected cells[1][2][3][4][5][6]. These antigen-MHC complexes are central to immune memory and vaccine efficacy, but are not considered discrete molecular drug targets in the classical sense.
Not directly targeted by drugs; immune mechanisms include T-cell recognition, cytolytic activity against antigen-presenting cells
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