MEI-HWEI CHANGHONG-YUAN HSUYEN-HSUAN NIKEH-SUNG TSAIPING-ING LEEPEI-JER CHENHsu Y.-L.Chen D.-S.2021-07-032021-07-0319980168-8278https://www.scopus.com/inward/record.uri?eid=2-s2.0-84984541485&doi=10.1016%2fS0168-8278%2898%2980337-1&partnerID=40&md5=82969213aa4e352ad7e1398edaf11382https://scholars.lib.ntu.edu.tw/handle/123456789/568830Background/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<0.05). Conclusions: These observations suggest that this mutant is selected by host immune pressure, but is not an initiator in the loss of immune tolerance during childhood chronic hepatitis B virus infection.[SDGs]SDG3aminotransferase; hepatitis B surface antigen; hepatitis B(e) antibody; hepatitis B(e) antigen; mutant protein; adolescent; article; child; childhood disease; female; hepatitis B; Hepatitis B virus; human; immunological tolerance; infant; major clinical study; male; newborn; polymerase chain reaction; priority journal; seroconversion; stop codon; vertical transmission; virus carrier; virus gene; virus transmissionjournal article10.1016/S0168-8278(98)80337-196721642-s2.0-84984541485