Objective: To explore the mechanism of hepatitis B virus (HBV) inhibiting M1 macrophages to promote immune escape, and to provide targets and strategies for antiviral therapy. Methods: The human monocyte cell line THP-1 was induced into M1 macrophages with PMA+LPS+IFN-γ. Cell morphological changes and the expressions of CD68, CD86, HLA-DR and functional molecules IL-1β, IL-6, TNF-α in M1 macrophages were detected by flow cytometry and RT-qPCR to identify M1 macrophages. HBV stable replication cell line HepG2.2.15 were co-cultured with M1 macrophages, and the expression of HBV-DNA was detected by qPCR. The expression of CD68, CD86 and HLA-DR were detected by flow cytometry. The expressions of functional molecules TLR4, NLRP3, Caspase-1, pro-caspase-1, caspase-1 p20, IL-1β and IL-18 in M1 macrophages were determined by RT-qPCR and Western blot. Apoptosis rate was detected by flow cytometry, and the expression of apoptosis related protein cleaved-caspase-3 was determined by Western blot. Results: THP-1 was successfully induced to differentiate into M1 macrophages. M1 macrophages inhibited HBV replication (P<0.05). HBV inhibited the expressions of CD68, CD86 and HLA-DR in M1 macrophages(P<0.01). HBV inhibited the expressions of TLR4, NLRP3, Caspase-1, caspase-1 p20, IL-1β and IL-18 in M1 macrophages (P<0.01). HBV induced M1 macrophage apoptosis (P<0.05). Conclusion: HBV inhibits M1 macrophages and their functional molecules TLR4, NLRP3 and downstream factors, reduces the synthesis and secretion of inflammatory factors, induces apoptosis, and then promotes immune escape, resulting in the persistence and replication of HBV in the body. [ABSTRACT FROM AUTHOR]