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Monocytes are crucial players in innate immunity. The human cytomegalovirus (CMV) infection has significant impacts on monocyte effector functions and gene expression. CMV, a β-herpesvirus, disrupts key monocyte roles, including phagocytosis, antigen presentation, cytokine production, and migration, impairing their ability to combat pathogens and activate adaptive immune responses. CMV modulates monocyte gene expression, decreasing their capacity for antigen presentation and phagocytosis while increasing pro-inflammatory cytokine production, which can contribute to tissue damage and chronic inflammation. CMV also alters monocyte migration to sites of infection while promoting trans-endothelial migration, thus aiding viral dissemination. Additionally, the virus affects reactive oxygen species (ROS) production, thereby contributing to end-organ disease associated with CMV infection. Overall, these changes enhance viral persistence during acute infection and facilitate immune evasion during latency. We highlight the clinical significance of these disruptions, particularly in immunocompromised patients such as transplant recipients, where the modulation of monocyte function by CMV exacerbates risks for infection, inflammation, and graft rejection. An understanding of these mechanisms will inform therapeutic strategies to mitigate CMV-related complications in vulnerable populations.