Abstract: Objective To study the correlation of serum monokine induced by IFN-γ （Mig），regulated upon activation normal T-cell expressed and secreted factors（RANTES） and IL-9 levels to HBV pre-C /BCP mutation and their influences on the response to Peg-IFN-α therapy in patients with HBeAg-positive hepatitis B. Methods A total of 43 HBeAg positive patients with CHB who received Peg-IFN-α therapy were enrolled in this study. Serum HBV DNA was extracted from peripheral blood，and polymerase chain reaction（PCR） was performed to sequence the Pre-C/BCP gene fragments. Serum levels of Mig，RANTES and IL-9 were detected by using cytometric bead array （CBA）. Results The mutation （MT） of HBV Pre- C and/or BCP was positive in 19 （44.2%） patients，and the wild type was 24（55.8%） out of the 43 HBeAg-positive hepatitis B patients; the serum levels of RANTES and IL-9 were （3274.24±814.79） pg/mL and（9.40±0.89） pg/mL， respectively， in patients with HBV pre-C/BCP mutation, and were （2742.40±764.24） pg/mL and （10.78±2.73） pg/mL, respectively, in patients without HBV pre-C/BCP mutation，and the difference was statistically significant（P<0.05）；nine（47.4%） out of patients with and 4 （16.7%） out of those without viral mutation obtained complete response at the end of 48 week regimen（P<0.05）. The baseline level of serum Mig in patients with serum HBsAg decline at week 24 of Peg-IFN-α treatment was（138.17±96.57） pg/mL，and the baseline level in those without HBsAg decline was （89.74±78.25） pg/mL （P<0.05）；In patients with HBV pre-C/BCP mutation, the baseline level of IL-9 was （10.78±2.73） pg/mL，the levels at week 12 and 24 during the treatment were （8.83±1.94） pg/mL and （8.91±1.97） pg/mL，both significantly lower than the baseline（P<0.05）. Conclusion Serum level of IL-9 is closely associated with HBV Pre-C / BCP mutation，but not with anti-HBV efficacy of Peg-IFN-α treatment in HbeAg-positive patients with CHB. Higher baseline level of Mig could contribute to HBsAg decline after PegIFN-α therapy in CHB patients with HBV pre-C/BCP mutation.

Key words: Hepatitis B, Mutation, PEG-IFN-α, Interleukin 9, Monokine induced by IFN-γ