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Nucleic Acids Res:宿主限制因子与肠道病毒EV71相互作用方面新进展

2018-09-28 ipsvirus 病毒学界

该研究揭示了APOBEC3G(A3G)通过与病毒复制必需的PCBP1竞争结合EV71的5‘UTR序列,抑制EV71在宿主细胞中的复制及翻译,首次揭示了A3G对小RNA病毒的抑制作用,为A3G广谱抗病毒增加新成员。

近日,国际知名期刊Nucleic acids research在线发表了吉林大学第一医院艾滋病与病毒研究所张文艳教授团队题为" Enterovirus 71 antagonizes the inhibition of the host intrinsic antiviral factor A3G "的研究成果。该研究揭示了APOBEC3G(A3G)通过与病毒复制必需的PCBP1竞争结合EV71的5‘UTR序列,抑制EV71在宿主细胞中的复制及翻译,首次揭示了A3G对小RNA病毒的抑制作用,为A3G广谱抗病毒增加新成员。

研究背景

手足口病是世界范围内常见的儿童流行病,其传播速度较快,范围较广,人群普通易感。近几十年来,在全球多个国家和地区(特别是亚太地区)发生了多次大规模手足口病暴发流行,2008年我国卫生部将手足口病正式列入法定丙型传染病以检测管理,研究显示,手足口病其主要的病原体为EV71和CA16,其中,EV71可诱导重症患者的产生。然而,在手足口病流行情况越发严峻的同时,我们还缺乏抑制其病原体感染的特异性药物。那么进一步通过揭示抗病毒机制,寻找新靶点尤为重要。

结果速览

本研究中,研究者研究发现A3G抑制EV71并不依赖其著名的胞嘧啶脱氨酶活性,而是通过与翻译复合物中的成员PCBP1竞争结合EV71的5‘UTR,进而阻断了EV71调控病毒RNA的翻译和复制,达到抑制病毒的目的。另一方面, EV71的2C蛋白可通过诱导选择性自噬而达到特异性的降解A3G,从而突破其对病毒的限制。进一步揭示了宿主限制因子与肠道病毒EV71相互作用的机制。



Fig. EV71 2C antagonizes A3G via the autophagy–lysosome degradation pathway but not the proteasome pathway.

结 语

肠道病毒感染近年来一直严重威胁婴幼儿健康,本研究试图从宿主限制因子这一新视角为解决这一问题找到线索。研究结果表明宿主限制因子A3G与EV71的相互作用一方面提供了限制肠道病毒复制的靶点,一方面为肠道病毒与天然免疫的相关研究提供了新的思路。

吉林大学第一医院博士生李兆龙为文章的第一作者,张文艳教授为本文通讯作者。本研究得到国家自然科学基金项目(31270202、81672004、81701987)、科技部国家重大科学研究计划(973计划)子课题(2012CB911102)、吉林省科技厅、吉林大学科技创新团队项目以及吉林大学研究生创新研究计划的支持。

原始出处:Li Z1, Ning S1, Su X1, et al. Enterovirus 71 antagonizes the inhibition of the host intrinsic antiviral factor A3G. Nucleic Acids Res. 2018 Sep 21. 

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    2019-01-03 zhouqu_8
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    2019-01-29 xlxchina
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    2018-09-30 wincls
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    2018-09-30 ylz8405

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