Lindh M, Hannoun C, Dhillon A P, Norkrans G, Horal P
Department of Clinical Virology, Göteborg University, S-413 46 Göteborg, Sweden.
J Infect Dis. 1999 Apr;179(4):775-82. doi: 10.1086/314688.
Virus load and liver damage, as measured by quantitative polymerase chain reaction and histology activity index, were related to genotype and core promoter mutations in 43 chronic hepatitis B virus (HBV) carriers of East Asian origin. T-1762 mutants were more frequent in genotype C strains and were associated with more inflammation (P=.0036) and fibrosis (P=.0088) of the liver but not with hepatitis B e antigen (HBeAg) status or virus load. Conversely, precore mutations were associated with less liver inflammation (P=. 08), which was linked to HBeAg negativity and lower viral replication. Carriers with genotype C were more often HBeAg positive (P=.03) with precore wild type strains and more-severe liver inflammation (P=.009) than were those with genotype B. These findings suggest that pathogenic differences between genotypes may exist and that the T-1762 mutation may be useful as a marker for progressive liver damage but seem to contradict that down-regulation of HBeAg production is the major effect of this mutation.
通过定量聚合酶链反应和组织学活性指数测定，东亚裔43例慢性乙型肝炎病毒（HBV）携带者的病毒载量和肝损伤与基因型及核心启动子突变有关。T-1762突变体在C基因型毒株中更常见，并且与肝脏更多炎症（P = 0.0036）和纤维化（P = 0.0088）相关，但与乙肝e抗原（HBeAg）状态或病毒载量无关。相反，前核心突变与肝脏炎症较少（P = 0.08）相关，这与HBeAg阴性和较低的病毒复制有关。与B基因型携带者相比，C基因型携带者在前核心野生型毒株中更常出现HBeAg阳性（P = 0.03），且肝脏炎症更严重（P = 0.009）。这些发现表明不同基因型之间可能存在致病差异，并且T-1762突变可能作为进行性肝损伤的一个标志物，但这似乎与该突变的主要作用是下调HBeAg产生相矛盾。
