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Updated: Jun 23, 2026

Lentiviral Vector Preparation for Efficient Gene and MicroRNA Modulation of Peritoneal Cavity Tissue-Resident Macrophages In Vivo in Mice
Published on: February 16, 2024
Macrophages in oncoviral infections: from immune regulators to therapeutic targets
Ruixue Sang1,2, Qingchun Zhang2, Fang Wang3
1Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China.
Background:
Human oncoviruses infect host cells and drive tumorigenesis. Macrophages, as key innate immune cells, exhibit functional heterogeneity and polarization plasticity. They are broadly classified into proinflammatory M1 and anti-inflammatory M2 states, which determine their role in immunity and tissue homeostasis.
Methods:
We summarized the recent experimental and clinical studies on the interactions between macrophages and the major oncoviruses, including Epstein-Barr virus (EBV), Kaposi's Sarcoma-associated herpesvirus (KSHV), hepatitis B virus (HBV), hepatitis C virus (HCV), human T-cell leukemia virus type 1 (HTLV-1), and human papillomavirus (HPV). We focus on how viral proteins, non-coding RNAs, and extracellular vesicles reprogram macrophage functions and discuss emerging macrophage-targeted therapeutic strategies.
Results:
Oncoviruses drive macrophages toward pro-tumor M2 or dysfunctional M1 states by altering cytokine secretion, activating signaling pathways, such as cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) and nuclear factor kappa B (NF-κB), and reprogramming metabolic pathways. New therapeutic strategies targeting macrophages, including polarization modulation, bispecific antibodies, nanomedicine delivery systems, and immune checkpoint strategies, show promise in enhancing antiviral and antitumor immunity.
Conclusion:
Macrophages can sense various oncoviruses and play a role in oncovirus infection, chronic inflammation, and virus-driven tumorigenesis. Potential therapeutic strategies targeting macrophages offer new avenues for the precision treatment of oncovirus-associated diseases.
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