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REGULATION OF THE HUMAN BETA-INTERFERON GENE EXPRESSION BY HEPATITIS-B VIRUS.

机译：乙型肝炎病毒对人类β-干扰素基因表达的调节。

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摘要

Individuals chronically infected with hepatitis B virus (HBV) have a deficiency in the in vivo interferon response. To determine whether HBV suppresses the synthesis of human beta-interferon, a series of recombinant bovine papilloma virus (BPV) plasmids that contained the human beta-interferon gene and various fragments of HBV DNA were constructed. Mouse C127 fibroblast cells were transfected with various recombinant BPV plasmids and permanently transformed cell lines were established by geneticin sulfate G418 selection.;A hybrid gene in which the expression of the bacterial chloramphenicol acetyltransferase (CAT) gene is under the control of the regulatory region of the human beta-interferon gene was constructed. The expression of the CAT gene was inhibited not only by the entire HBV genome but also by the 1828 bp BamHI HBV DNA fragment. A frameshift mutation introduced within the structural gene of the core antigen abolishes the inhibitory activity. These results suggest that HBV suppresses the expression of the human beta-interferon by interacting in the same manner with the ;In addition, the 2755 bp BglII HBV DNA fragment containing the surface antigen gene and the ORF X was identified to have a transactivating activity in a transient DNA expression system. The transactivating activity was defined and attributed to the HBV X antigen gene. These results strongly suggest that transcription of the HBV X antigen gene is necessary for transactivation. (Abstract shortened with permission of author.).;To determine the stage of the synthesis of human beta-interferon that is inhibited by the product of the 1828 bp BamHI HBV DNA fragment, levels of human beta-interferon-specific RNA in the various transformed cell lines were measured. The level of RNA specific for human beta-interferon gene was decreased in only those transformed C127 cells that contained the 1828 bp BamHI HBV DNA fragment. Results of nuclear run-on experiments to detect the rate of transcription of the human beta-interferon gene indicate that the suppression of interferon synthesis by HBV occurs at the level of transcription.
机译：慢性感染乙型肝炎病毒（HBV）的个体体内干扰素反应不足。为了确定HBV是否抑制人β-干扰素的合成，构建了一系列包含人β-干扰素基因和各种HBV DNA片段的重组牛乳头瘤病毒（BPV）质粒。用各种重组BPV质粒转染小鼠C127成纤维细胞，并通过硫酸遗传G418选择建立永久转化的细胞系;杂合基因，其中细菌氯霉素乙酰基转移酶（CAT）基因的表达受CAT调控区的控制。人β干扰素基因被构建。 CAT基因的表达不仅受到整个HBV基因组的抑制，还受到1828 bp BamHI HBV DNA片段的抑制。在核心抗原的结构基因内引入的移码突变消除了抑制活性。这些结果表明HBV通过与HBV相同的相互作用而抑制了人β-干扰素的表达；此外，含有表面抗原基因和ORF X的2755 bp BglII HBV DNA片段被鉴定具有反式激活活性。瞬时DNA表达系统。定义了反式激活活性并将其归因于HBV X抗原基因。这些结果强烈提示HBV X抗原基因的转录对于反式激活是必需的。 （摘要在作者允许下缩短。）；确定受1828 bp BamHI HBV DNA片段的产物抑制的人β-干扰素的合成阶段，各种人β-干扰素特异性RNA的水平测量转化的细胞系。仅在包含1828 bp BamHI HBV DNA片段的那些转化的C127细胞中，人β-干扰素基因特异的RNA水平降低。用于检测人β-干扰素基因转录速率的核实验结果表明，HBV抑制干扰素合成的过程发生在转录水平。

著录项

  • 作者

    TWU, JR-SHIN.;

  • 作者单位

    Indiana University.;

  • 授予单位 Indiana University.;
  • 学科 Molecular biology.
  • 学位 Ph.D.
  • 年度 1987
  • 页码 201 p.
  • 总页数 201
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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