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Ebola Virus (EBOV) VP24 Inhibits Transcription and Replication of the EBOV Genome

机译:埃博拉病毒(EBOV)VP24抑制EBOV基因组的转录和复制

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摘要

The roles of Ebola virus (EBOV) VP24 in nucleocapsid (NC) formation and the effect of VP24 on transcription and replication of the viral genome during NC formation remain unknown. We therefore examined the effect of VP24 on the expression of a reporter gene (luciferase), viral RNA, and messenger RNA from the EBOV minigenome. VP24 inhibited the expression of luciferase and both RNAs in a dose-dependent manner, suggesting that VP24 inhibits transcription and replication of the EBOV genome. By contrast, FLAG-tagged VP24, which cannot support NC-like structure formation, did not appreciably decrease luciferase expression, indicating that association of VP24 with the ribonucleoprotein complex is required for inhibition. Glycoprotein and VP40 did not affect VP24-mediated inhibition of transcription and replication. Together, these results suggest that VP24 reduces transcription and replication of the EBOV genome by direct association with the ribonucleoprotein complex in virus-infected cells.
机译:埃博拉病毒(EBOV)VP24在核衣壳(NC)形成中的作用以及VP24在NC形成过程中对病毒基因组转录和复制的影响仍然未知。因此,我们检查了VP24对来自EBOV微型基因组的报道基因(荧光素酶),病毒RNA和信使RNA表达的影响。 VP24以剂量依赖的方式抑制萤光素酶和两个RNA的表达,表明VP24抑制EBOV基因组的转录和复制。相比之下,FLAG标记的VP24无法支持NC样结构的形成,并没有明显降低萤光素酶的表达,表明抑制作用需要VP24与核糖核蛋白复合物的缔合。糖蛋白和VP40不会影响VP24介导的转录和复制抑制。总之,这些结果表明,VP24通过与病毒感染细胞中的核糖核蛋白复合物直接缔合来减少EBOV基因组的转录和复制。

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  • 来源
    《Journal of Infectious Diseases》 |2007年第2期|S284-S290|共7页
  • 作者单位

    Department of Pathobiological Sciences School of Veterinary Medicine University of Wisconsin Madison;

    International Research Center for Infectious Diseases University of Tokyo Tokyo;

    Division of Virology Department of Microbiology and Immunology Institute of Medical Science University of Tokyo Tokyo;

    Core Research for Evolutional Science and Technology (CREST) Japan Science and Technology Agency Saitama Japan;

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