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Significance of pre‐S region–defective hepatitis B virus that emerged during exacerbation of chronic type B hepatitis
Author(s) -
Minami Masahito,
Okanoue Takeshi,
Nakajima Etsuro,
Yasui Koichiro,
Kagawa Keizo,
Kashima Kei
Publication year - 1993
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840170406
Subject(s) - hepatitis b virus , virus , virology , biology , hepatitis b virus dna polymerase , antibody , mutation , stop codon , hepatitis b , microbiology and biotechnology , immunology , genetics , gene
A defective form of the hepatitis B virus has been found in a patient with chronic type B hepatitis. Sequence analysis of the viral DNA after polymerase chain reaction amplification revealed a 117–base pair deletion (nucleotides 3129–53, subtype adr). This deletion includes the initiation codon of the pre‐S2 region and a newly created in‐frame stop codon in the pre‐S1 region (nucleotide 3055) located 230 base pairs downstream from the pre‐S1 initiation codon. This virus coexisted with the wild‐type virus during the exacerbation period, as evidenced by an elevation of serum transaminase levels. It was not detected in the stable period, and the blood chemistry results were normal. We assayed antibodies against the mutationrelated region by enzyme immunoassay in serial serum samples to clarify the mechanism of the emergence of this variant virus. Antibodies against the pre‐S2 region were negative; however, the antibody response against the pre‐S1 epitopes coincided with the appearance of the variant virus. These findings suggest that an activated T‐cell and B‐cell response had developed against the pre‐S1 region during hepatic inflammation in this patient and that, consequently, selection occurred for a pre‐S antigen–defective mutant strain of the virus that might be resistant to such an immune response. (H EPATOLOGY 1993;17:558–563.)