| Objective To study the characteristics of hepatitis B virus(HBV) precore G1896A mutation and basal core promoter (BCP) A1762T/G1764A mutation or the united mutation of them (G1896A and A1762T/G1764A mutation together) between HBeAg-negative and HBeAg-positive patients with Chronic Hepatitis B (CHB). To analyze the clinical significance of HBV precore G1896A mutation and basal core promoter A1762T/G1764A mutation or the united mutation of them in patients with HBeAg-negative CHB, to explore the relationships between HBV precore G1896A mutation and basal core promoter A1762T/G1764A mutation with cytokine in patients with CHB.Methods Sera from 120 CHB patients with HBVDNA(+) and 60 healthy person were collected. They were divided into three groups: group A was 60 CHB patients with HBeAg-negative which included 19 mild patients, 29 moderate patients and 12 serious patients; Group B was 60 CHB patients with HBeAg-positive which included 22 mild patients, 28 moderate patients and 10 serious patients; Group C was 60 healthy person. Viral loads of HBVDNA in sera of group A and group B were demonstrated using real-time quantification PCR.The rates of precore G1896A mutation and BCP A1762T/G1764A mutation in CHB patients in group A and group B were detected using polymerase chain reaction (PCR) and sequencing the products directly.120 CHB patients were also divided into mutation group and non-mutation group according to HBV precore and basal core promoter sequence results.The levels of IFN-γor IL-10 in serum of groups mutation , non-mutation and healthy control were measured by enzyme linked immunosorbent assay(ELISA).Results 48 patients of HBV mutation were detected in group A and 24 patients of HBV mutation were detected in group B .The incidences of precore region G1896A mutations were 38.3%(23/60)and 16.7%(10/60)(х2=7.06, P =0.008) in group A and group B respectively. The incidences of A1762T/G1764A mutation were 16.7% (10/60)and 23.3%(14/60)(х2=0.83, P =0.361) in the same patients respectively.The rate of the united mutation was 25% only in group A (х2=17.14, P =0.000). The levels of HBVDNA viral loads in the groups of G1896A mutation and A1762T/G1764A mutation and the united mutation in patients with HBeAg-negative were(5.87±0.85)lgcopies/ml(,5.84±0.82)lgcopies/ml(,5.95±0.50)lgcopies/ml,they were higher than those of non-mutation groups(4.50±0.71)lgcopies/ml,(4.46±0.69)lgcopies/ml,(4.75±0.94)lgcopies/ml. t=7.58, t=7.94, t=4.42 respectively, P <0.05. In the mild, moderate and serious CHB patients with HBeAg-negative, the mean ranks of the groups G1896A mutation and A1762T/G1764A double mutation and the united mutation (34.25, 37.40, 40.37) were higher than those in the non-mutation groups (24.02, 25.57 ,27.21; P<0.05). The serum levels of IFN-γin the mutation group were(102.33±27.20)pg/ml ,they were significantly higher than those in the non-mutation group(79.18±16.43)pg/ml and the healthy control group(35.77±4.23)pg/ml, ( P <0.01) .The serum levels of IL-10 in the mutation group were(28.13±7.00)pg/ml,they were also significantly higher than those in the non-mutation group (13.91±5.42)pg/ml and the healthy control gruop(13.68±2.27)pg/ml, ( P <0.01).Conclusions (1) The mutation of G1896A and the united mutation may be a major mechanism which lead HBVDNA positive and HBeAg negative.(2) The mutations of G1896A and A1762T/G1764A may be associated with the severity of HBeAg-negative CHB .(3) The mutations of G1896A or A1762T/G1764A may increase the levels of IFN-γand IL-10. |
PDF Full Text Request