[Distribution of pre-core A83 point mutation in hepatitis B virus infections].
We designed a mispairing primer, which could introduce a Bsu36I restriction site into the amplified fragment of A83 mutant. Following PCR, the 102bp was diagnosed by the restriction endonuclease, and the variation was detected by demonstration of 82bp and 20bp bands on gel electrophoresis (RFLP). With the method, 77 cases of acute and chronic HBV infections were analysed. Among those, 31 (65%) mutants were detected in 48 anti-HBe-positive cases, and in 29 HBeAg-positive cases, 11 (38%) were co-infected with mutated and wild isolates. No pre C defect was found in acute hepatitis B and chronic asymptomatic carriers, suggesting that mutation occurs only after immune selection. The HBeAg defective variant appears to be involved in the loss of virus tolerance, and therefore in the pathogenesis of acute exacerbation of chronic carriage as demonstrated in this study. The various chronic liver diseases had an approximate mutation frequency, and it seems that A83 mutation nearly makes HBV infection persist.
Luo
K X
KX
Nanfang Hospital, Guangzhou.
Yang
J
J
Li
X H
XH
D000940:Antigenic Variation; D001483:Base Sequence; D002353:Carrier State; D006509:Hepatitis B / Q000235:genetics*; D006513:Hepatitis B e Antigens / Q000235:genetics; D006515:Hepatitis B virus / Q000235:genetics*; D006521:Hepatitis, Chronic / Q000235:genetics; D006801:Humans; D008969:Molecular Sequence Data; D017354:Point Mutation; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length
D006513:Hepatitis B e Antigens