OBJECTIVE: To investigate the genetic variation and typing of hepatitis B virus (HBV) in patients with chronic hepatitis B in relation to HBeAg status. METHODS: Fluorescence quantitative polymerase chain reaction (PCR) was employed to detect serum HBV DNA in patients with chronic hepatitis B negative for HBeAg. Real-time fluorescent PCR and PCR-reverse dot blot hybridization were used to detect HBV genotypes and mutations, respectively. RESULTS: Of the 389 patients, 214 (55.01%) were positive and 175 (44.99%) were negative for HBV DNA; 102 (26.22%) had a HBV DNA copy number of 1×10(3), and 41 (10.54%) had a copy number of 1×10(4) (Χ(2)=226.6729, P<0.001). Of the 21 patients with a HBV DNA load of 1×10(5), 15 (71.43%) were found to have precore mutations, and 11 (52.38%) had basic core promoter (BCP) mutations; a higher HBV-DNA load was associated with an increased incidence of HBV mutations. In the 214 patients positive for HBV DNA, HBV genotypes A, B, C, D and the mixed type were found in 6 (2.80%), 84 (39.25%), 106 (49.53%), and 7 (3.27%), and 11 (5.14%) patients, who showed precore mutation rates of 16.67% (1 case), 36.90% (31 cases), 44.34% (47 cases), 0, and 0, and BCP mutation rates of 0, 19.05% ( 16 cases), 26.42% (28 cases), 0, and 0, respectively, demonstrating significant differences in HBV mutations between the genotype groups (P<0.001). CONCLUSION: HBeAg-negative and HBV DNA-positive patients with chronic hepatitis B have a relatively low HBV replication level, and HBV DNA load is associated with HBV mutations. The B and C genotypes are more likely to have HBV mutations in HBeAg-negative patients.
OBJECTIVE: To investigate the genetic variation and typing of hepatitis B virus (HBV) in patients with chronic hepatitis B in relation to HBeAg status. METHODS: Fluorescence quantitative polymerase chain reaction (PCR) was employed to detect serum HBV DNA in patients with chronic hepatitis B negative for HBeAg. Real-time fluorescent PCR and PCR-reverse dot blot hybridization were used to detect HBV genotypes and mutations, respectively. RESULTS: Of the 389 patients, 214 (55.01%) were positive and 175 (44.99%) were negative for HBV DNA; 102 (26.22%) had a HBV DNA copy number of 1×10(3), and 41 (10.54%) had a copy number of 1×10(4) (Χ(2)=226.6729, P<0.001). Of the 21 patients with a HBV DNA load of 1×10(5), 15 (71.43%) were found to have precore mutations, and 11 (52.38%) had basic core promoter (BCP) mutations; a higher HBV-DNA load was associated with an increased incidence of HBV mutations. In the 214 patients positive for HBV DNA, HBV genotypes A, B, C, D and the mixed type were found in 6 (2.80%), 84 (39.25%), 106 (49.53%), and 7 (3.27%), and 11 (5.14%) patients, who showed precore mutation rates of 16.67% (1 case), 36.90% (31 cases), 44.34% (47 cases), 0, and 0, and BCP mutation rates of 0, 19.05% ( 16 cases), 26.42% (28 cases), 0, and 0, respectively, demonstrating significant differences in HBV mutations between the genotype groups (P<0.001). CONCLUSION: HBeAg-negative and HBV DNA-positive patients with chronic hepatitis B have a relatively low HBV replication level, and HBV DNA load is associated with HBV mutations. The B and C genotypes are more likely to have HBV mutations in HBeAg-negative patients.