Pathogenic human herpesviruses infect virtually all humans, establishing lifelong infection with no cure. Herpes simplex virus type 1 (HSV-1), otherwise known as oral herpes, creates a range of infection outcomes including asymptomatic infection, orofacial sores, and life-threatening encephalitis. The standard drugs for management of HSV-1 infection disrupt viral DNA replication, but recent emergence of drug-resistant HSV-1 strains highlights a need to identify new antiviral targets. Upon infection of a host cell, HSV-1 forms liquid-liquid phase-separated viral replication compartments (VRCs) in the nucleus where all steps of viral replication and packaging occur. However, the molecular mechanisms contributing to the formation and maintenance of HSV-1 VRCs are uncharacterized. In this project, we investigate the effect of the cellular kinase DYRK3 on HSV-1 VRCs. DYRK3 has a role in dissolving cellular phase-separated condensates during mitosis, releasing mitotic regulators and preventing formation of aberrant condensates. Since DYRK3 targets condensates with a similar structure to HSV-1 VRCs, it is possible that DYRK3 could impair or regulate viral replication, potentially by dissolving VRCs. In this project, we visualize the effect of DYRK3 on VRCs in live cells using confocal laser scanning microscopy with fluorophore-tagged proteins. Through transfection and infection, we observe the spatio-temporal integrity of phase-separated VRCs in conditions of both DYRK3 overexpression and inhibition. Our study of HSV-1 VRC regulation by DYRK3 will reveal insights into the cellular response to viral infection and potentially uncover new antiviral targets.