BACKGROUND: Occult infection of hepatitis B virus (HBV) has important impacts on both public health and clinical medicine. OBJECTIVES: To characterize the sequences of HBV S region in a chronic carrier with occult HBV infection. STUDY DESIGN: Serological markers for HBV were tested by commercial kits. Western blotting was performed to detect HBsAg. PCR was used to amplify HBV S region; the resultant products were sequenced directly and cloned and then sequenced. RESULTS: Tests with commercial kits showed that the carrier was HBsAg negative yet HBeAg positive. HBsAg was positive in Western blotting analysis. Although anti-HBs titers were as high as 5356-11,578mIU/ml, serum HBV DNA was positive, ranging from 370 to 491copies/ml. Wild type and mutant HBV coexisted in circulation. The mutant virus had mutations in both preS2 and S genes: the preS2 ATG mutated to ATA, and the S gene had a 15-nucleotide repeat insertion in the a determinant. By Blast search in the GenBank, the mutant virus had not been identified before. Nevertheless, the carrier had no signs of liver dysfunction during follow-up period. CONCLUSION: We identified a novel mutant HBV coexisted with wild type virus in a carrier with negative HBsAg and positive HBeAg and high level of anti-HBs.
BACKGROUND: Occult infection of hepatitis B virus (HBV) has important impacts on both public health and clinical medicine. OBJECTIVES: To characterize the sequences of HBV S region in a chronic carrier with occult HBV infection. STUDY DESIGN: Serological markers for HBV were tested by commercial kits. Western blotting was performed to detect HBsAg. PCR was used to amplify HBV S region; the resultant products were sequenced directly and cloned and then sequenced. RESULTS: Tests with commercial kits showed that the carrier was HBsAg negative yet HBeAg positive. HBsAg was positive in Western blotting analysis. Although anti-HBs titers were as high as 5356-11,578mIU/ml, serum HBV DNA was positive, ranging from 370 to 491copies/ml. Wild type and mutant HBV coexisted in circulation. The mutant virus had mutations in both preS2 and S genes: the preS2 ATG mutated to ATA, and the S gene had a 15-nucleotide repeat insertion in the a determinant. By Blast search in the GenBank, the mutant virus had not been identified before. Nevertheless, the carrier had no signs of liver dysfunction during follow-up period. CONCLUSION: We identified a novel mutant HBV coexisted with wild type virus in a carrier with negative HBsAg and positive HBeAg and high level of anti-HBs.