Mutations in the basic core promotor and the precore region of hepatitis b virus and their selection in children with fulminant and chronic hepatitis B

摘要: The involvement of precore stop codon 1896-A and base exchanges in the AT-rich region at positions 1762 1764 hepatitis B core promotor has been controversely discussed adults with fulminant B. Because no data are currently available on children, we analyzed basic (BCP) children chronic BCP were sequenced directly after cloning from mothers infants. Thirteen suffered liver disease, 6 whom treated interferon alfa (IFN-alpha). All 13 patients seroconverted e antigen (HBeAg) to antibodies (anti-HBe), sera before seroconversion. Nine vertically infected infants developed a course occurrence (1762-T/1764-A, 7.7%) (1896-A, 7.7%; 1899-A, 15%) mutations was rare. A genotype shift D observed 3 development anti-HBe. high number detected those Eight nine showed G-A exchange 1896/97 (89%), 1899 (56%), and/or nucleotide (nt) (56%) (78%). virus strains belonged D, whereas only surviving infant, D-to-A detected. Hepatitis (HBV) DNA clones examined babies 5 mothers. Our results heterogeneous population 4 In contrast, homogeneous emerged According our data, analysis revealed striking presence mutants (FH) when compared clinically inapparent anti-HBe-positive (P <.002), which could be one factor pathogenesis children.