Mechanisms and Therapeutic Implications of Galectins Regulating Epstein–Barr Virus Infection

Epstein–Barr virus (EBV) is a ubiquitous herpesvirus associated with a broad spectrum of malignancies and immune-mediated disorders, and growing evidence highlights the importance of host glycan–lectin interactions in shaping viral persistence and immune escape. Among these, galectins have emerged as key regulators of the EBV life cycle, influencing viral attachment, latency maintenance, lytic reactivation, and the remodeling of the tumor microenvironment. Galectin-1, -3, and -9 exhibit context-dependent functions that collectively modulate oncogenic signaling pathways, T‑cell exhaustion, regulatory T‑cell expansion, and innate immune sensing. Recent clinical studies further suggest that circulating galectins and galectin-enriched exosomes may serve as non-invasive biomarkers for disease progression and prognosis in EBV-associated malignancies. Despite these advances, major knowledge gaps remain regarding member-specific functions, compensatory galectin networks, and the spatiotemporal dynamics of galectin regulation during infection. Targeting the galectin–glycan axis therefore represents a promising frontier for host-directed antiviral and anticancer therapies, with the potential to disrupt viral latency, restore antiviral immunity, and improve clinical outcomes in EBV-driven diseases.