Human cytomegalovirus replication (HCMV replication)

Human cytomegalovirus (HCMV) replication is the coordinated biological process by which the virus duplicates its double-stranded DNA genome and assembles new virions within a host cell [Griffiths et al., 2021]. This process involves several essential viral enzymes that serve as key therapeutic targets, including the UL54 DNA polymerase, the UL97 protein kinase, and the terminase complex (UL56/UL89/UL51) [StatPearls, 2023]. Antiviral drugs such as ganciclovir and foscarnet target the UL54 DNA polymerase to inhibit viral DNA synthesis, while newer agents like letermovir target the UL56 subunit of the terminase complex to prevent viral DNA packaging and maturation [FDA, 2017]. Maribavir is a more recent addition that inhibits the UL97 kinase, which is crucial for viral nuclear egress and assembly [FDA, 2021]. HCMV replication is a significant clinical concern in immunocompromised populations, such as transplant recipients and individuals with HIV/AIDS, and is a major cause of congenital infections [CDC, 2020]. Clinical management relies on monitoring CMV DNA viral load as a biomarker for replication activity and to guide the duration of antiviral therapy [Ljungman et al., 2019].

Other names

HCMV replication cycleCytomegalovirus DNA replicationHCMV viral replicationCMV replication

Inhibition of viral DNA polymerase (UL54), inhibition of viral terminase complex (UL56), and inhibition of viral protein kinase (UL97) [Griffiths et al., 2021; FDA, 2021].