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Abstract
Human cytomegalovirus (HCMV) is a pervasive β-herpesvirus that establishes lifelong persistence within the host by adopting a latent state in hematopoietic progenitor cells (HPCs). Periodic reactivation from latency poses significant risks to immunocompromised individuals and contributes to HCMV-associated disease, yet the viral and host mechanisms governing this process remain incompletely defined. Among HCMV’s gene products, a subset of virally encoded G protein-coupled receptors (vGPCRs) have emerged as critical regulators of latency and reactivation. This dissertation investigates the molecular signaling properties, interactomes, and functional consequences of two vGPCRs, US28 and UL78, in order to delineate how HCMV manipulates host pathways to persist and reactivate from latent infection.