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Sequential analyses of the mutations in the core upstream and precore regions of hepatitis B virus genome in anti‐HBe positive‐carriers developing acute exacerbation
Author(s) -
Nishizono Akira,
Kohno Kazuhiro,
TakitaSonoda Yoshiko,
Hiraga Masaharu,
Terao Hideo,
Fujioka Toshio,
Nasu Masaru,
Mifune Kumato
Publication year - 1997
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199711)53:3<266::aid-jmv15>3.0.co;2-f
Subject(s) - virology , hepatitis b virus , point mutation , asymptomatic carrier , mutation , biology , exacerbation , virus , orthohepadnavirus , hepadnaviridae , mutant , hepatitis b , asymptomatic , genetics , medicine , gene , immunology , pathology
The nucleotide sequences of the core upstream and precore regions (371 nucleotide length, nt. 1604‐1974) of hepatitis B virus (HBV) were analysed sequentially in three subjects who were positive serorogically for anti‐HBe and had acute clinical exacerbation after immunosuppressive treatment. These patients were asymptomatic HBV carriers before therapy. The results revealed that the mutant with an 8‐bp deletion (nt. 1768–1775) located in the basic core promoter region was dominant in the asymptomatic HBV carrier phase in two of three subjects. After exacerbation, however, such mutant clones possessing 8‐bp deletion disappeared or decreased in number and were replaced by the clones possessing a precore stop codon mutation G to A (nt. 1896) or by the clones possessing additional contiguous point mutations A to T (nt. 1762) and G to A (nt. 1764) and a new point mutation C to T (nt. 1653). Possible relationships between acute exacerbation of liver function accompanied by mutation and the transition of the dominant clones were discussed. J. Med. Virol. 53:266–272, 1997. © 1997 Wiley‐Liss, Inc.