Human cytomegalovirus-infected cells (CMV-infected cells)

Human cytomegalovirus (HCMV)-infected cells are host cells, such as myeloid progenitors, endothelial cells, and epithelial cells, that have been colonized by the virus, serving as the primary site for viral replication, assembly, and the establishment of lifelong latency [1.1.4, 1.4.5]. Upon infection, these cells undergo significant molecular reprogramming, expressing viral proteins like pp65, IE1, and US28 that can be detected on the cell surface or presented via MHC molecules, making the infected cell a target for the immune system and specialized therapies [1.2.1, 1.4.4]. Traditional antiviral treatments focus on inhibiting the viral replication machinery within these cells by targeting enzymes like DNA polymerase or the terminase complex [1.3.3, 1.3.5]. More recently, advanced immunotherapies, including CMV-specific T-cells and TCR-like antibodies, have been developed to selectively recognize and eliminate infected cells by targeting viral peptides presented on the cell surface [1.4.2, 1.4.3]. CMV-infected cells are a major clinical concern in immunocompromised populations, where uncontrolled viral reactivation can lead to severe end-organ disease, and they have also been implicated in the progression of certain malignancies like glioblastoma [1.4.1, 1.4.4].

Other names

HCMV-infected cellsCMV-positive cellsCytomegalovirus-infected host cells

Drugs targeting CMV-infected cells primarily work by inhibiting viral DNA polymerase (e.g., ganciclovir, foscarnet, cidofovir) to prevent viral DNA synthesis [1.3.1, 1.3.3]. Letermovir inhibits the viral terminase complex (UL56/UL51/UL89), preventing the cleavage and packaging of viral DNA [1.3.3, 1.3.5]. Maribavir inhibits the UL97 protein kinase, which is essential for viral DNA replication and nuclear egress [1.3.4, 1.3.5]. Immunotherapies like CMV-specific T-cells (e.g., posoleucel) or TCR-like antibodies recognize viral peptides (e.g., pp65) presented on the cell surface via MHC class I molecules, leading to the direct cytotoxic destruction of the infected cell [1.2.1, 1.4.2, 1.4.3].