慢性病毒感染及其在塑造肿瘤免疫微环境中的作用

Chronic viral infections, such as HBV, HCV, EBV, and HPV, contribute to tumorigenesis not only through direct oncogenic effects but also by reshaping the tumor immune microenvironment (TIME) via complex immunoregulatory mechanisms. These infections enhance immune suppression and promote metastasis. Viruses induce the accumulation of regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and immunosuppressive cytokines, while driving CD8 + T cell exhaustion and impairing NK cell function, creating an immune environment favorable for tumor survival. Chronic inflammation, pro-angiogenic factors, and signals mediated by exosomes and microvesicles further remodel local and distant microenvironments, forming a "pre-metastatic niche" that supports tumor cell colonization and metastasis.

Key signaling pathways, including NF-κB, STAT3, PD-1/PD-L1, and TGF-β, are persistently activated by viral proteins such as HBx and LMP1, reinforcing immunosuppression and metastasis. Based on these mechanisms, combined strategies of antiviral therapy with immune checkpoint inhibitors (ICIs) or targeting exosomes and immunosuppressive pathways show potential to enhance antitumor immunity and limit metastasis.

A deeper understanding of the virus-immune-metastasis axis and related biomarkers may provide precise immunotherapeutic strategies for virus-associated cancers and improve patient outcomes.