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A Cytomegalovirus (CMV) infected cell refers to a host cell, typically of myeloid, endothelial, or epithelial lineage, that has been successfully invaded by Human Cytomegalovirus (HCMV) [10, 14]. These cells serve as the site for the complex HCMV replication cycle, which involves the coordinated expression of immediate-early, early, and late viral genes, as well as significant remodeling of the host cell environment [5, 13]. In clinical practice, the infected cell is the functional target of direct-acting antiviral therapies that inhibit essential viral enzymes located within the cell, such as the DNA polymerase (UL54), the protein kinase (UL97), or the terminase complex (UL56) [4, 8, 12]. Furthermore, infected cells are the primary target for the host's cellular immune response and advanced immunotherapies; viral proteins like pp65 and IE1 are processed and presented on the cell surface via MHC Class I molecules, allowing recognition and destruction by CMV-specific cytotoxic T-lymphocytes [2, 6]. Persistence of these infected cells, especially in a latent state within hematopoietic progenitor cells, allows the virus to cause lifelong infection and potentially reactivate during periods of immunosuppression, leading to severe diseases such as pneumonia, retinitis, and gastrointestinal disease [1, 10, 16].
Inhibition of viral DNA polymerase (UL54) to block DNA synthesis, inhibition of the viral terminase complex (UL56) to prevent DNA packaging, inhibition of viral protein kinase (UL97) to disrupt capsid egress and replication, and T-cell mediated recognition and lysis of cells presenting viral epitopes (e.g., pp65, IE1) on the cell surface.
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