siderable liver damage.6-8 A TAG stop codon mutation in the Hepatitis B e antigen (HBeAg) is considered to be a terminal part of the precore region prevents synthesis of major target for the immune response in chronic hepatiHBeAg and explains the absence of HBeAg in serum in most tis B. The G r A mutation at nucleotide 1896 may mediate of these patients. 9,10 Selection of this nucleotide (nt) 1896 G r viral escape by creating a TAG stop codon in the precore A mutation (nt position from the unique EcoR1 site) may occur region, thus preventing HBeAg production. This mutain the immunoreactive stage of hepatitis B, because HBeAgtion frequently evolves during HBe seroconversion if derived epitopes are thought to be important targets for the thymine, but rarely if cytosine, is present in position immune response against hepatitis B virus (HBV).
11-131858. Applying a combination of polymerase chain reacThe preference for the 1896 G r A mutation, as compared tion (PCR) and restriction enzyme action, we have studwith other point mutations that prevent HBeAg production, ied the relation of the TAG mutation and the nucleotide is explained by the fact that the base-pairing in the stem of (nt) 1858 variants to liver damage assessed by histology the pregenomic RNA loop and the specific functional seactivity index (HAI) scoring in 175 chronic hepatitis B quences of the precore region restrict the variability. 14-20 The virus (HBV) carriers. A TAG mutation was found in 68 TAG mutation is tolerated, because a U-1858 may form a of 71 (96%) of HBeAg-negative carriers infected with a base pair with either a G or A in nt position 1896. In strains T-1858 strain, but not in any of 33 carriers infected excluwith a C-1858, however, a G r A mutation at nt 1896 does sively with a C-1858 strain. Four patients showed a mutanot evolve, because it would considerably impair encapsidation of the precore start codon, and 2 had a TAA stop tion and replication. 18 This explains why the mutation is unmutation at codon 2. HBeAg-positive infection with a common among carriers of western European and North mixture of wild-type and TAG mutant virus indicated American origin, who usually are infected with genotype A active liver damage, because 8 of 9 (89%) of such patients strains, which carry C-1858. 18 Infection with the precore TAG had a Knodell HAI ¢8. In HBeAg-negative stage, both mutant has been associated with severe chronic hepatitis, 21 inflammation and fibrosis were more pronouced in carfulminant hepatitis, 22-24 severe recurrent HBV infection after riers infected with wild-type HBV compared with preliver transplantation, 25 and it may influence the response to core mutants. C-1858 strains were associated with more interferon therapy. 26,27 The described association with severe inflammation and fibrosis compared with T-1858 strains.chronic hepatitis has been questioned, because mutant HBV C-1858 strains were found in 71% of northern European, has also been found in healthy carriers of HBV. [28][29][30][31][32] The rela-17% of southern Europ...
