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Analysis of the Hepatitis B virus precore and ORF‐X sequences in patients with antibody to hepatitis B e antigen with and without normal ALT levels
Author(s) -
Cabrerizo María,
Bartolomé Javier,
Iñigo Elena R.,
LópezAlcorocho Juan Manuel,
Cotonat Teresa,
Carreño Vicente
Publication year - 1998
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(199812)56:4<294::aid-jmv2>3.0.co;2-u
Subject(s) - virology , hepatitis b virus , polymerase chain reaction , biology , hepatitis b virus dna polymerase , mutation , genotype , hepadnaviridae , virus , hepatitis b , microbiology and biotechnology , dna , antibody , gene , immunology , genetics
Serum samples from 20 anti‐hepatitis B e antigen‐positive patients with and without normal alanine aminotransferase (ALT) levels who had serum hepatitis B virus (HBV) DNA detectable only by polymerase chain reation (PCR) were examined. Viral DNA was amplified by PCR, using primers that encompassed precore and ORF‐X regions and sequenced directly, to investigate whether mutations in the nucleotide sequences of X and precore gene regions of HBV‐DNA might be responsible for the difference in the activity of disease and in the levels of viral replication. The HBV‐DNA concentration in patients with abnormal ALT levels was higher than in those with normal ALT. The amount of HBV‐DNA correlated with the ALT levels ( P < 0.05). Seventy‐two percent of patients had HBV‐DNA harboring the 1896 precore stop mutation, and there was a negative correlation between the percentage of precore mutant genotype and the HBV‐DNA concentration ( P < 0.05). Thirty percent of patients had mutations in ORF‐X. Patients with ORF‐X mutations had lower levels of HBV‐DNA than those who had wild‐type virus. The presence of mutations in precore and X regions may be related to a low HBV‐DNA concentration and reduced biochemical activity in patients with anti‐HBe. J. Med. Virol. 56:294–299, 1998 . © 1998 Wiley‐Liss, Inc.