Twu J S, Lee C H, Lin P M, Schloemer R H
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis 46223.
Proc Natl Acad Sci U S A. 1988 Jan;85(1):252-6. doi: 10.1073/pnas.85.1.252.
To determine whether hepatitis B virus (HBV) regulates the expression of the human beta-interferon gene, a series of recombinant bovine papilloma virus plasmids containing the human interferon gene and various fragments of the HBV genome were constructed and used to transform C127 cells, a murine fibroblast line. Analysis of the DNA from transformed C127 cells indicated that the interferon gene was intact and that the plasmids replicated as stable multicopy elements. The 1828-base-pair BamHI HBV DNA fragment containing the core antigen gene, but not the 2755-base-pair Bgl II HBV DNA fragment encoding both the surface antigen and the X antigen, suppressed the production of human beta-interferon. No effect by any of the recombinant plasmids on the synthesis of murine interferon was detected. The suppression of human beta-interferon by HBV occurs via a trans-acting factor. A frameshift mutation within the HBV core gene alleviates the inhibitory activity; thus we infer that the core protein is this factor or is crucially associated with this activity.
为了确定乙肝病毒（HBV）是否调控人β-干扰素基因的表达，构建了一系列含有人类干扰素基因和HBV基因组不同片段的重组牛乳头瘤病毒质粒，并用于转化小鼠成纤维细胞系C127细胞。对转化的C127细胞的DNA分析表明，干扰素基因完整，且质粒作为稳定的多拷贝元件进行复制。包含核心抗原基因的1828碱基对的BamHI HBV DNA片段，而非编码表面抗原和X抗原的2755碱基对的Bgl II HBV DNA片段，抑制了人β-干扰素的产生。未检测到任何重组质粒对小鼠干扰素合成有影响。HBV对人β-干扰素的抑制作用通过反式作用因子发生。HBV核心基因内的移码突变减轻了抑制活性；因此我们推断核心蛋白就是这个因子或与该活性密切相关。
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