A Transgenic Mouse Model of the Chronic Hepatitis B Surface Antigen Carrier State

乙型肝炎表面抗原 生物 乙型肝炎病毒 病毒学 HBcAg 抗原 乙型肝炎病毒β前体 七鳃鳗科 抗原性 基因 分子生物学 转基因小鼠 HBeAg 病毒 转基因 免疫学 乙型肝炎病毒DNA聚合酶 遗传学
作者
Francis V. Chisari,Carl A. Pinkert,David R. Milich,P Filippi,A. McLachlan,Richard D. Palmiter,Ralph L. Brinster
出处
期刊:Science [American Association for the Advancement of Science]
卷期号:230 (4730): 1157-1160 被引量:286
标识
DOI:10.1126/science.3865369
摘要

In an attempt to establish a model of the healthy carrier state in hepatitis B virus (HBV) infections, transgenic mice expressing HBV genes were produced. Fertilized one-cell eggs were microinjected with subgenomic fragments of HBV DNA containing the coding regions for the HBV surface antigen (HBsAg) and pre-S and X antigens. Either the normal (HBV) or metallothionein promoters were used to obtain expression of the HBV genes. There was no evidence of viral replication or tissue pathology. The integrated HBV DNA sequences were inherited in a normal Mendelian fashion. Three of 16 transgenic mice expressed HBV-encoded gene products to which they were immunologically tolerant. Expression was not tissue specific and may be influenced by the genomic integration site and cellular factors. Both HBsAg and pre-S antigen were detectable within the cytoplasm of hepatocytes and renal tubular epithelial cells. High serum concentrations of HBsAg were detectable and the secreted product appeared authentic as judged by mean density, morphology, mean particle diameter, polypeptide composition, and antigenicity. The absence of tissue pathology in these immunologically tolerant animals supports the hypothesis that cellular injury under these conditions is not a direct consequence of expression of the pre-S or HBs regions of the HBV genome.
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