from Anamaris M. Colberg-Poley and Chad D. Williamson writing in Cytomegaloviruses: From Molecular Pathogenesis to Intervention:
As with most DNA viruses, which require nuclear and cytoplasmic phases of virion maturation, proper and coordinated trafficking of viral proteins is crucial for the CMV lifecycle. Trafficking of CMV proteins enables jumpstarting its infection, partly determines whether lytic or latent infection is established, promotes nuclear and cytoplasmic assembly of virions, and enhances their stability and egress. To allow complex processes including viral DNA replication, packaging, nuclear and cytoplasmic egress, trafficking of CMV proteins is temporally and spatially regulated by modifications, particularly phosphorylation, and by interactions between viral or cellular proteins. Thus, orchestrated recruitment and colocalization of necessary components to enable functions are assured. In addition to conventional nuclear and cytoplasmic trafficking of viral proteins, HCMV encodes an antiapoptotic UL37 exon 1 protein or viral mitochondria-localized inhibitor of apoptosis, which circuitously traffics from the ER to mitochondria and through ER subdomains known as mitochondria-associated membranes. By this unconventional trafficking, HCMV is able to commandeer ER-mitochondrial cross-talk as well as mitochondrial functions, metabolism, antiviral responses, and apoptosis. The importance of proper intracellular trafficking of some key HCMV proteins such as those required for its DNA replication and assembly is supported by the deleterious effects of their inhibition on HCMV permissive growth.
Further reading: Cytomegaloviruses: From Molecular Pathogenesis to Intervention