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Epstein-Barr virus (EBV) is one of the most pervasive viruses worldwide, and EBV infection is inextricably linked to a multitude of lymphoid and epithelial neoplasms. EBV is responsible for the advancement of malignant disease by modifying the tumor microenvironment (TME), which is a sophisticated and evolving system that facilitates tumor growth, invasion, and metastasis. EBV infection has a profound impact on the cellular and noncellular components that constitute the TME. Our review presents a summary of the composition of the EBV-remodeled TME, with a particular focus on EBV-induced functional phenotypes in non-tumor cells. Furthermore, we discuss the potential for reversing EBV-driven TME remodeling as a therapeutic strategy for treating the malignancies associated with EBV infection.
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Li et al. (2025) studied this question.
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