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Objectives:To investigate the molecule immunology mechanism of HBV persistent infection, we observed the expressions of TLR3, MDA-5 and RIG-I in macrophage cells, which were interacted with HBV.Method:THP-1 cells were induced into macrophage-like cells after PMA treatment. Macrophage-like cells were collected at 2h,4h,12h and 24h after HBV treatment in order to test the expressions of Toll like receptor 3(TLR3), melanoma differentiation-associated gene-5(MDA-5) and retinoic acid inducible gene-I(RIG-I) by real time PCR. Then, macrophage-like cells were treated with poly I:C in the presence or absence of HBV. The supernatants were collected at 4h after poly I:C treatment. The expression of interferon-beta (IFN-β) in the supernatants was measured by ELISA.Result:In HBV treated groups, the expressions of TLR3 at the above four time points were lower than those in control group, and at each time point, the expressions of TLR3 in HBV high load groups were lower than those in low load groups (F= 123.64, 24.49,6.69 and 7.63, all P<0.01). In high viral load groups, the expressions of MDA-5 and RIG-I at four time points were low when compared with low viral load groups (F=36.44,48.57,46.59 and 12.77; 67.68,74.54,18.31and 26.16; all P<0.01). The secretions of IFN-βafter poly I:C treatment in positive control group were higher than those in HBV treated groups (F=78.42, P<0.01), and the productions of IFN-βafter poly I:C treatment in HBV low load groups were higher than those in high load groups, and the concentration of IFN-P in each group was (497.2±43.7), (294.2±48.4), (92.5±12.3) and (40.4±9.9)pg/ml, respectively.Conclusion: HBV inhibits the expressions of TLR3, MDA-5 and RIG-I and the secretion of IFN-β. This may be one of the roles in the escape from innate immunity.
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