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乙型肝炎病毒RNA通过类Rev途径的输出:再生肝抑制因子IkappaBα的抑制作用

Export of hepatitis B virus RNA on a Rev-like pathway: inhibition by the regenerating liver inhibitory factor IkappaB alpha.

作者信息

Roth J, Dobbelstein M

机构信息

ZIM, Gastroenterologie, Klinikum der Universität Marburg, Germany.

出版信息

J Virol. 1997 Nov;71(11):8933-9. doi: 10.1128/JVI.71.11.8933-8939.1997.

Abstract

Nuclear export of hepatitis B virus (HBV) RNA is mediated by a specific RNA element but, in contrast to lentivirus genomic RNA, does not depend on viral proteins. We show that nonetheless, the export of HBV RNA can be blocked by competitive inhibitors of Rev-mediated lentivirus RNA export, suggesting that the export pathways of both viral species share components and might be driven by the same nuclear export machinery. HBV RNA export is also inhibited by overexpression of IkappaB alpha, as reported previously for the export of human immunodeficiency virus RNA. Since IkappaB alpha is strongly overexpressed during liver regeneration, its inhibition of HBV RNA export might contribute to elimination or silent persistence of HBV.

摘要

乙型肝炎病毒(HBV)RNA的核输出由特定的RNA元件介导,但与慢病毒基因组RNA不同的是,它不依赖病毒蛋白。我们发现,尽管如此,HBV RNA的输出可被Rev介导的慢病毒RNA输出的竞争性抑制剂所阻断,这表明这两种病毒的输出途径共享一些成分,并且可能由相同的核输出机制驱动。如先前关于人类免疫缺陷病毒RNA输出的报道一样,IkappaBα的过表达也会抑制HBV RNA的输出。由于IkappaBα在肝脏再生过程中会强烈过表达,其对HBV RNA输出的抑制作用可能有助于HBV的清除或隐匿性持续存在。

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The hepatitis B virus PRE contains a splicing regulatory element.乙型肝炎病毒PRE包含一个剪接调节元件。
Nucleic Acids Res. 2006 Jan 12;34(1):353-63. doi: 10.1093/nar/gkj440. Print 2006.

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