Precore stop codon mutant in chronic hepatitis B virus infection in children: its relation to hepatitis B e seroconversion and maternal hepatitis B surface antigen

• Published in: Journal of hepatology 1998-06, Vol.28 (6), p.915-922
• Main Authors: Chang, Mei-Hwei, Hsu, Hong-Yuan, Ni, Yen-Hsuan, Tsai, Keh-Sung, Lee, Ping-Ing, Chen, Pei-Jer, Hsu, Ya-Ling, Chen, Ding-Shinn
• Format: Article
• Language: English
• Subjects: Adolescent; Amplified created restriction site; Biological and medical sciences; Carrier State - virology; Child; Child, Preschool; Codon, Terminator - genetics; Female; Follow-Up Studies; Hepatitis B e antigen; Hepatitis B e Antigens - blood; Hepatitis B e seroconversion; Hepatitis B Surface Antigens - blood; Hepatitis B Surface Antigens - genetics; Hepatitis B virus - genetics; Hepatitis B, Chronic - blood; Human viral diseases; Humans; Infant; Infant, Newborn; Infectious Disease Transmission, Vertical; Infectious diseases; Male; Medical sciences; Point Mutation; Polymerase Chain Reaction; Precore stop codon mutant; Pregnancy; Pregnancy Complications, Infectious - virology; Restriction Mapping; Viral diseases; Viral hepatitis
• ISSN: 0168-8278; 1600-0641
• DOI: 10.1016/S0168-8278(98)80337-1

Background/Aims: The aims of this study were to investigate the significance of the precore stop codon mutant in the natural course of hepatitis B virus infection in children, and the influence of maternal transmission. Methods: Sequential sera from 80 hepatitis B virus carrier children both before and after e seroconversion during long-term follow-up were studied using the polymerase chain reaction-amplification created restriction site method. Direct sequencing of the precore region was performed in 89 sera from 32 of the 80 children. Results: The precore stop codon mutant coexisting with wild strain was found in 10% of children initially, and later in 25% of children before e seroconversion. After e seroconversion, wild type was still present in 75% and mutant in 39% of children at the end of follow-up. The mutant alone was present in 15% of anti-HBe positive children without concomitant aminotransferase elevation. Children with earlier emergence of this mutant tended to have higher peak aminotransferase levels. This mutant emerged less frequently in children of hepatitis B virus carrier mothers (37.5%) than in those of non-carrier mothers (65%) ( p