Human cytomegalovirus (HCMV) is a ubiquitous pathogen that causes morbidity and mortality in immuno-compromised people, and severe defects to newborn infants. Efficient HCMV replication requires successful cellular entry into a host, genome duplication, virion assembly, and release. HCMV remodels the entire host organelle landscape to engineer construction of the cytoplasmic megastructure termed the viral assembly complex (vAC). Morphologically, the vAC in HCMV-infected cells presents as an enlarged kidney-bean-shaped nucleus, juxtaposed to a Golgi-derived vesicle ring that encapsulates and sequesters endosome-derived vesicles. vAC function has been linked to facilitating virion maturation, whereby genome-containing nucleocapsids are thought to traffic through the vAC for tegumentation, followed by budding into a host-derived organelle to provide the outer viral membrane. The biogenesis of the vAC largely remains a molecular mystery, and we study this intriguing viral factory from both host and viral perspectives, using a multidisciplinary approach. For example, we are currently attempting to disassemble this structure using a library of 150 single open reading frame HCMV mutants. We also use CRISPR to gene edit host cells to define secretory pathways being hijacked by the virus. Another strategy we pursue uses various proteomic approaches to identify critical host-viral interactions that mediate secondary envelopment. All together, we anticipate this knowledge will provide novel insights that can be harnessed to impede HCMV maturation.