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Objective To investigate the effect and mechanism of HBV 一 stimulated HTR8 一 S/Vneo mitochondrial antiviral signaling protein (MAVS) signaling pathway on the immune response of peripheral blood mononuclear cell (PBMC) to hepatitis B vaccine. Methods The HTR8 - S/Vneo were co 一 incubated with serum of HBV - DNA positive patients. MAVS siRNA transfection was hereby applied for silencing of MAVS and MAVS plasmid transfection was applied for overexpression of MAVS in HTR8 一 S/Vneo. We then cocultured them with human immune cells assembly PBMC and subsequently stimulated with hepatitis B vaccine. The mRNA and protein expression levels of MAVS, NF - kB, pNF - kB, IRF3 and pIRF3 in HTR8 一 S/Vneo were detected by reverse transcription 一 quantitative real 一 time PCR (RT 一 qPCR) and flow cytometry (FCM). The levels of IL - 2, IL - 6, IFN 一 p and IL 一 17 were detected by enzyme - linked immunosorbent assay (ELISA), and the proportion of CD4+ T cell were detected by flow cytometry. The data were analyzed for t test. Results HBV down 一 regulated the mRNA expression levels of MAVS, NF - kB, IRF3 (£ 二 6. 66, P 二 0. 003; £ 二 14. 18, P < 0. 001; £ 二 3. 70, P 二 0. 021) and the protein expression levels of MAVS, NF - kB, pNF - kB(£ 二 3. 42, P = 0. 042; £ 二 4. 23, P = 0. 013; £ 二 4. 86, P - 0. 008), and inhibited the production of IFN - p(£ 二 9. 83, P = 0. 010). Silencing MAVS down 一 regulated the mRNA and protein expression of MAVS(£ 二 31. 20, P < 0. 001; £ 二 6. 53, P = 0. 023), inhibited the expression of IFN - p(£ 二 5. 46, P =0. 032), and reduced the proportion of CD4+ T cells in PBMC(£ 二 9. 07, P = 0. 001). Overexpression of MAVS induced IFN 一 B production(£ 二一 34. 26, P < 0. 001; t - -5. 11, P = 0, 036), but the proportion of CD4 * T cells did not show significant effect (/二 一 0. 73, P 二 0. 506). Conclusion HBV can inhibit the MAVS signaling pathway in HTR8 一 S/Vneo. Overexpression of MAVS could promote the immune response to hepatitis B vaccine in PBMC. [ABSTRACT FROM AUTHOR]