| Objective To explore the change of the cellular immunity by comparing the dynamic changes of interferon-γ(IFN-γ) and interleukin-4 (IL-4) in the serum of patients with e antigen-positive chronic hepatitis B (CHB) treated with ETV versus adefovir dipivoxil (ADV), and to try to explore the influence of immunity by the treatment of antiviral. To find practical markers to predict the effect of therapy.Methods Sixty hepatitis B e antigen positive and nucleoside-naive CHB patients were randomized into two groups:32 patients received ETV 0.5mg once daily were entered into an ETV arm, and 28 patients received ADV 10mg once daily were entered into an ADV arm. All patients were completed 48weeks therapy. At different time (before therapy and 12 week,24 week,48 week of therapy), the serum level of IFN-γand IL-4 of each patient were determined by ELISA.Results At pretreatment,12 week,24 week and 48 week of therapy, the level of serum IFN-γin patients treated with ETV was significantly higher than that in patients treated with ADV (17.72±4.51pg/mL,25.77±7.82pg/mL,29.83±6.57pg/mL 33.06±6.28pg/mL vs 15.92±4.16pg/mL,21.23±7.89pg/mL,24.09±7.89pg/mL 27.26±8.29pg/mL, respectively, P=0.009). The level of serum IL-4 in patients treated with ETV was significantly lower than patients treated with ADV (34.47±6.84pg/mL,25.80±8.35pg/mL,18.73±9.32pg/mL,13.53±11.28pg/mL vs 33.41±5.66pg/mL,30.17±7.08pg/mL,26.25±10.56pg/mL,22.90±13.42pg/mL, P=0.019). At the 48 week of treatment HBV DNA negative rate (HBV DNA< 31gcopies/mL) was 81%(26/32) in entecavir-treated patients and was 54%(15/28) in adefovir-treated patient (P<0.05). At baseline,12 week,24 week and 48 week of therapy, the level of serum IFN-γin response group were significantly higher than no response group (HBV DNA≥31gcopies/mL), there was 17.14±4.59pg/mL, 26.11±8.16pg/mL,30.14±6.70pg/mL,33.08±6.88pg/mL vs 16.32±4.03pg/mL, 18.36±4.96pg/mL,20.71±8.16pg/mL,24.45±6.31pg/mL, respectively, P<0.001). The mean of serum IL-4 was significantly greater in response group compared with no response group and at baseline,12 week,24 week and 48 week of therapy, there was 33.68±5.44pg/mL,24.75±5.99pg/mL,16.66±5.95pg/mL,10.24±6.11pg/mL vs 34.63±7.94pg/mL,34.52±7.91pg/mL,34.28±7.84pg/mL,34.43±7.57pg/mL in two groups respectively (P<0.001). At the 48 week of treatment a total of 9 patients achieved e antigen seroconversion, the rate of HBeAg seroconversion was 15%(9/60). The rate of HBeAg seroconversion was 15.6%(5/32) in entecavir-treated patients and was 14.3%(4/28) in adefovir-treated patient, there was no statistically significant in two groups (P=1.000). The level of serum IFN-y in seroconversion group were significantly higher than no seroconversion group and at baseline,12 week,24 week and 48 week of therapy, there was 19.17±7.63pg/mL,29.76±5.35pg/mL, 34.63±4.77pg/mL,36.58±5.89pg/mL vs 16.48±3.53pg/mL,22.57±6.40pg/mL, 26.04±6.70pg/mL,29.25±6.82pg/mL, respectively (P<0.01). The mean of serum IL-4 was significantly greater in seroconversion group compared with no seroconversion group and at baseline,12 week,24 week and 48 week of therapy, there was 34.07±7.12pg/mL,23.11±8.58pg/mL,14.92±7.25pg/mL,8.48±4.83pg/mL vs 33.96±6.21pg/mL,28.68±7.72pg/mL,23.55±10.68pg/mL,19.41±13.56 pg/mL in two groups respectively (P<0.05).Conclusions(1) After antiviral treatment, the level of serum IFN-ywas significantly higher and the level of serum IL-4 was significantly lower than that at baseline in patients treated with ETV and the results are associated with viral load decline caused by antiviral therapy.(2) There was similar HBeAg antigen seroconversion rates ETV and ADV groups suggesting that immune factors plays an important role in the seroconversion. The mean of serum IFN-y and IL-4 was significantly greater in conversion group compared with no conversion group indicated antiviral therapy can promote HBeAg antigen seroconversion by suppress viral replication.(3) The cellular immune response of patients with hepatitis B was resumed in some extent after ETV therapy, which may result from the reduction of viral load and restoration of CD4+T cell reactivity.
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