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黄病毒 NS1' 是日本脑炎病毒血清群的一种产物,是核糖体移码的结果,在病毒神经侵袭性方面发挥作用。

NS1' of flaviviruses in the Japanese encephalitis virus serogroup is a product of ribosomal frameshifting and plays a role in viral neuroinvasiveness.

机构信息

Centre for Infectious Disease Research, School of Chemistry and Molecular Biosciences, The University of Queensland, St. Lucia, Brisbane, QLD 4072, Australia.

出版信息

J Virol. 2010 Feb;84(3):1641-7. doi: 10.1128/JVI.01979-09. Epub 2009 Nov 11.

DOI:10.1128/JVI.01979-09
PMID:19906906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2812330/
Abstract

Flavivirus NS1 is a nonstructural protein involved in virus replication and regulation of the innate immune response. Interestingly, a larger NS1-related protein, NS1', is often detected during infection with the members of the Japanese encephalitis virus serogroup of flaviviruses. However, how NS1' is made and what role it performs in the viral life cycle have not been determined. Here we provide experimental evidence that NS1' is the product of a -1 ribosomal frameshift event that occurs at a conserved slippery heptanucleotide motif located near the beginning of the NS2A gene and is stimulated by a downstream RNA pseudoknot structure. Using site-directed mutagenesis of these sequence elements in an infectious clone of the Kunjin subtype of West Nile virus, we demonstrate that NS1' plays a role in viral neuroinvasiveness.

摘要

黄病毒 NS1 是一种非结构蛋白,参与病毒复制和固有免疫反应的调节。有趣的是,在感染日本脑炎病毒血清群黄病毒时,通常会检测到一种较大的 NS1 相关蛋白 NS1'。然而,NS1' 是如何产生的,以及它在病毒生命周期中扮演什么角色,尚未确定。在这里,我们提供实验证据表明 NS1' 是核糖体 -1 移码事件的产物,该事件发生在 NS2A 基因起始附近的保守滑链七核苷酸基序处,并受下游 RNA 假结结构的刺激。我们使用西尼罗河病毒 Kunjin 亚型的感染性克隆中的这些序列元件的定点突变,证明 NS1' 在病毒神经侵袭性中发挥作用。

相似文献

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NS1' of flaviviruses in the Japanese encephalitis virus serogroup is a product of ribosomal frameshifting and plays a role in viral neuroinvasiveness.黄病毒 NS1' 是日本脑炎病毒血清群的一种产物,是核糖体移码的结果,在病毒神经侵袭性方面发挥作用。
J Virol. 2010 Feb;84(3):1641-7. doi: 10.1128/JVI.01979-09. Epub 2009 Nov 11.
2
A conserved predicted pseudoknot in the NS2A-encoding sequence of West Nile and Japanese encephalitis flaviviruses suggests NS1' may derive from ribosomal frameshifting.西尼罗河病毒和日本脑炎黄病毒编码 NS2A 的序列中一个保守的预测假结表明 NS1' 可能源自核糖体移码。
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Recode-2: new design, new search tools, and many more genes.Recode-2:全新设计,全新搜索工具,以及更多基因。
Nucleic Acids Res. 2010 Jan;38(Database issue):D69-74. doi: 10.1093/nar/gkp788. Epub 2009 Sep 25.
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A conserved predicted pseudoknot in the NS2A-encoding sequence of West Nile and Japanese encephalitis flaviviruses suggests NS1' may derive from ribosomal frameshifting.西尼罗河病毒和日本脑炎黄病毒编码 NS2A 的序列中一个保守的预测假结表明 NS1' 可能源自核糖体移码。
Virol J. 2009 Feb 5;6:14. doi: 10.1186/1743-422X-6-14.
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West Nile virus nonstructural protein 1 inhibits TLR3 signal transduction.西尼罗河病毒非结构蛋白1抑制Toll样受体3信号转导。
J Virol. 2008 Sep;82(17):8262-71. doi: 10.1128/JVI.00226-08. Epub 2008 Jun 18.
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Antibody recognition of cell surface-associated NS1 triggers Fc-gamma receptor-mediated phagocytosis and clearance of West Nile Virus-infected cells.细胞表面相关NS1的抗体识别触发Fc-γ受体介导的吞噬作用并清除西尼罗河病毒感染的细胞。
J Virol. 2007 Sep;81(17):9551-5. doi: 10.1128/JVI.00879-07. Epub 2007 Jun 20.
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pknotsRG: RNA pseudoknot folding including near-optimal structures and sliding windows.pknotsRG:RNA假结折叠,包括近最优结构和滑动窗口
Nucleic Acids Res. 2007 Jul;35(Web Server issue):W320-4. doi: 10.1093/nar/gkm258. Epub 2007 May 3.
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In situ reactions of monoclonal antibodies with a viable mutant of Murray Valley encephalitis virus reveal an absence of dimeric NS1 protein.单克隆抗体与墨累谷脑炎病毒活突变体的原位反应显示不存在二聚体NS1蛋白。
J Gen Virol. 2007 Apr;88(Pt 4):1175-1183. doi: 10.1099/vir.0.82609-0.
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A single amino acid substitution in the West Nile virus nonstructural protein NS2A disables its ability to inhibit alpha/beta interferon induction and attenuates virus virulence in mice.西尼罗河病毒非结构蛋白NS2A中的单个氨基酸替换使其丧失抑制α/β干扰素诱导的能力,并减弱了病毒在小鼠中的毒力。
J Virol. 2006 Mar;80(5):2396-404. doi: 10.1128/JVI.80.5.2396-2404.2006.
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Antibodies against West Nile Virus nonstructural protein NS1 prevent lethal infection through Fc gamma receptor-dependent and -independent mechanisms.针对西尼罗河病毒非结构蛋白NS1的抗体通过Fcγ受体依赖性和非依赖性机制预防致死性感染。
J Virol. 2006 Feb;80(3):1340-51. doi: 10.1128/JVI.80.3.1340-1351.2006.
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Adv Virus Res. 2003;59:99-140. doi: 10.1016/s0065-3527(03)59004-2.