Analysis of wild-type and e antigen-defective hepatitis B viruses during the course of a short-term corticosteroid therapy in chronic hepatitis B
✍ Scribed by Manabu Daikoku; Keisuke Nakata; Keisuke Hamasaki; Akio Ido; Kazuhiko Nakao; Yuji Kato; Michiaki Koga; Michitami Yano; Shigenobu Nagataki
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 568 KB
- Volume
- 47
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Hepatitis B virus (HBV), with a G‐to‐A point mutation at nucleotide 83 in the precore region (mutant HBV83), accounts for most cases of hepatitis B e antigen (HBeAg)‐defective HBV. However, it is still not clear how mutant HBV83 is associated with HBe seroconversion. Twenty‐six HBeAgpositive patients with chronic hepatitis B who received oral prednisolone (30 mg/day) for 3 weeks were studied to clarify the prevalence of mutant HBV83 during the treatment using polymerase chain reaction with a restriction fragment length polymorphism assay. Twelve (46%) patients seroconverted to anti‐HBe 1 year after treatment, whereas 14 (54%) did not. The proportion of mutant HBV83 to whole HBV remained unchanged in both groups during an acute exacerbation induced by withdrawal of corticosteroids. Among 12 anti‐HBe‐0seroconverted patients, five (56%) of nine patients with only wild‐type HBV at baseline developed detectable levels of mutant HBV83 while all three patients with a mixed viral population of wild‐type HBV and mu tant HBV83 at baseline developed a higher pro portion of mutant HBV83 one year after treat ment. In contrast, these changes were observed in only one (14%) of seven who failed to seroconvert. The results indicate that a flare‐up of hepa titis precedes emergence or selection of mutant HBV83, followed by HBe seroconversion in patients with chronic hepatitis B. © 1995 WiIey‐Liss, Inc.