Tumor cells are known for being able to evade immune system surveillance, a hallmark of malignancy. Complicated immune escape mechanisms in the tumor microenvironment (TME) provide favorable conditions for tumor invasion, metastasis, treatment resistance, and recurrence. Epstein-Barr virus (EBV) infection is closely related to the pathogenesis of nasopharyngeal carcinoma (NPC), and the co-existence of EBV-infected NPC cells and tumor-infiltrating lymphocytes represents a distinctive, highly heterogeneous, and suppressive TME that supports immune escape and promotes tumorigenesis. Understanding the complex interaction between EBV and NPC host cells and focusing on the immune escape mechanism of TME may help to identify specific immunotherapy targets and to develop effective immunotherapy drugs.