Abstract
Objective To analyze the variations of surface(S)region, basic core promoter (BCP) and precore (preC) regions in genomes of hepatitis B virus (HBV) from patients with coexistence of hepatitis B surface antigen (HBsAg) and hepatitis B surface antibody (anti-HBs). Methods S region, BCP and preC regions in genomes of HBV were amplified and sequenced in 62 HBV-infected patients including 27 HBsAg-positive/anti-HBs-positive patients (double positive group) and 35 HBsAg-positive/anti-HBs-negative patients (single positive group). The sequencing results and amino acid variants in these regions were analyzed. Difference of means between groups was compared by t test. Sample rate and variation rate were compared by chi-square test. Results One hundred and fifty-six amino acids mutations within the S region were detected in 27 patients of double positive group and 100 mutations in 35 patients of single positive group. The mutation rate in double positive group was significantly higher than those in single positive (2.56% vs 1.26%, χ2=32.07, P<0.05). The amino acid variants in double positive group were much higher than those in single positive group within major hydrophilic region (MHR), especially in the first loop area of a-determinant in S region (4.76% vs 1.02%, χ2=11.58, P<0.05). The mutation rate of A1762T/G1764A in BCP in double positive group was significantly higher than those in single positive group (59.3% vs 28.6%, χ2=5.895, P<0.05). The mutation rate of A1846T in preC region was higher in double positive group than those in single positive group (40.7% vs 17.1%, χ2=4.265, P<0.05). The mutation rate of A1762T/G1764A+ G1896A in double positive group was also higher than that in single positive group (37.0% vs 14.3%, χ2=4.302, P<0.05). Conclusions The mutation rates of S region, especially in the first loop area within a-determinant, BCP and preC regions which are related with hepatocellular carcinoma development in HBsAg and anti-HBs double positive group are higher than those in HBsAg single positive group in chronic HBV infected patients. Key words: Hepatitis B virus; Hepatitis B surface antigens; Hepatitis B antibodies; Genes; Mutation
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