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Emergence and takeover of precore‐stop mutant prior to exacerbation of e antigen‐negative chronic hepatitis B after withdrawal of lamivudine therapy
Author(s) -
Yeh ChauTing,
Lin WeiPin,
Hsu ChaoWei,
Chang MingLing,
Lin ShiMing,
Sheen IShyan
Publication year - 2006
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/jmv.20639
Subject(s) - lamivudine , virology , hbeag , hepatitis b virus , hbcag , medicine , exacerbation , hepatitis b , population , hepatitis , immunology , virus , hbsag , environmental health
Although hepatitis B virus (HBV) precore‐stop mutant (nonsense mutation at codon 28) is usually isolated from patients with hepatitis B e antigen (HBeAg)‐negative hepatitis, it is unclear whether the mutant is the cause of the hepatitis flare or it is a consequence of necroinflammation. Using the amplification‐created restriction site method, the ratios of precore‐stop mutant were measured in serial serum samples obtained from three patients experiencing HBeAg‐negative hepatitis after withdrawal of lamivudine therapy. In all three patients, the precore‐stop mutant emerged and took over the viral population at least 2 months prior to the hepatitis exacerbations. After the onset of exacerbation, transient elevation of serum HBV‐DNA was observed, which was followed by progressive decrease of the ratio of precore‐stop mutant as well as normalization of serum transaminases. The present data indicate that at least in some patients, the precore‐stop mutant is the cause but not the consequence of the flare of HBeAg‐negative hepatitis. J. Med. Virol. 78:906–910, 2006. © 2006 Wiley‐Liss, Inc.