Kobayashi Mariko, Arase Yasuji, Ikeda Kenji, Tsubota Akihito, Suzuki Yoshiyuki, Saitoh Satoshi, Kobayashi Masahiro, Suzuki Fumitaka, Akuta Norio, Hosaka Tetsuya, Someya Takashi, Matsuda Marie, Sato Junko, Takagi Kimiko, Miyakawa Yuzo, Kumada Hiromitsu
Research Institute for Hepatology, Toranomon Hospital, Tokyo, Japan.
Intervirology. 2003;46(3):157-63. doi: 10.1159/000071456.
Factors influencing the resolution of persistent hepatitis B virus (HBV) infection were sought for.
The loss of hepatitis B surface antigen (HBsAg) from serum was correlated with mutations in HBV DNA for a hepatitis B e antigen (HBeAg)-minus phenotype in patients infected with HBV genotype C and positive for HBeAg at presentation.
HBeAg turned negative in all the 22 patients in whom HBV infection resolved, but only in 11 of the 25 patients with severe liver diseases (100 vs. 44%, p = 0.0001). The precore wild type (G1896) persisted significantly more frequently in the 22 patients in whom HBV infection resolved than in the 11 patients who developed decompensated liver cirrhosis or hepatocellular carcinoma (15/22 or 68% vs. 1/11 or 9%, p = 0.005). The double mutation in the core promoter (T1762/A1764) was comparably frequent in the two groups of patients at presentation (14/22 or 64% vs. 7/11 or 64%) and >15 years thereafter (18/22 or 82% vs. 10/11 or 91%).
The precore wild type (G1896) would seem to facilitate the resolution of HBV infection, while the precore mutant (A1896) may induce severe liver diseases in patients with HBeAg-positive chronic hepatitis who have lost HBeAg from serum.
