A case-control study for early prediction of hepatitis B e antigen seroconversion by hepatitis B virus DNA levels and mutations in the precore region and core promoter

✍ Scribed by Takahiro Yamaura; Eiji Tanaka; Akihiro Matsumoto; Akinori Rokuhara; Koji Orii; Kaname Yoshizawa; Yuzo Miyakawa; Kendo Kiyosawa

• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 124 KB
• Volume: 70
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.10429

✦ Synopsis

Abstract

Factors influencing and predictive of seroconversion from hepatitis B e antigen (HBeAg) to antibody (anti‐HBe) were sought in a case‐control study of 61 patients with chronic hepatitis B who had been observed from 5 years before to 1 year after seroconversion, and 32 patients who did not seroconvert during the entire 6‐year period. Almost all of the patients (96%) were infected with HBV genotype C. HBV DNA levels began to decrease 3 years before seroconversion in the seroconverters, while they remained high in the non‐converters. The frequency of precore mutation and the loss of HBeAg (A1896) started to increase 1 year before in the converters, and became significantly higher at seroconversion (23 vs. 3%, P = 0.030) than that in the non‐converters. Double mutation in the core promoter (T1762/A1764) was more common in the seroconverters than in the non‐converters 5 years before seroconversion (48 vs. 28%), and became significantly more frequent at seroconversion (65 vs. 41%, P = 0.046). Seroconversion occurred in 75% of the patients with at least HBV DNA levels <5.5 logarithmic equivalents/mL; precore mutation in 20% or more of HBV DNA; or core promoter mutation. Seroconversion occurred in 50% of those patients within 1 year, 88% within 2 years, and 93% within 5 years. These results indicate that a decrease in HBV DNA levels and mutations in the precore region and the core promoter were associated significantly and complementarily with seroconversion, and each of them or a combination thereof was predictive of seroconversion years ahead. J. Med. Virol. 70:545–552, 2003. © 2003 Wiley‐Liss, Inc.