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机构地区:[1]黑龙江中医药大学基础医学院,哈尔滨150040 [2]中国疾病预防控制中心病毒病预防控制所传染病预防控制国家重点实验室,北京102206 [3]齐齐哈尔医学院,黑龙江齐齐哈尔161006
出 处:《疾病预防控制通报》2013年第4期84-87,90,共5页Bulletin of Disease Control & Prevention(China)
基 金:传染病重大专项(2011ZX10004-001)和重点实验室发展基金(2011SKLID104)资助
摘 要:目的探究小RNA病毒入侵宿主细胞后,对细胞蛋白质翻译的影响。方法通过归纳整理相关的研究进展,总结出小RNA病毒入侵真核细胞后抑制宿主蛋白合成的几种机制。结果小RNA病毒可以通过裂解真核细胞翻译起始因子,对翻译起始因子或其结合蛋白的去磷酸化,以及阻止翻译起始复合物的形成等途径,抑制了宿主细胞的蛋白产生,同时依靠内部核糖体进入位点(IRES),进行病毒自身的蛋白合成。结论小RNA病毒通过其非结构蛋白的作用,迅速有效地抑制了宿主细胞的蛋白合成。Objective To explore effect on translation of host cell protein after picornavirus invaded the host cell. Methods Related research progresses were reorganized to summarize several mechanisms of inhibition of host protein syn- thesisthe after picornavirus invaded eukaryotic cells of the host. Results Host cell's own proteins would be inhibited promptly and efficiently, and at the same time virus could synthetize themselves' proteins by internal ribosome entry site (IRES). These progresses happened by several ways, such as cracking translation initiation factors of eukaryotic cells, dephos- phorylating translation initiation factors or their binding proteins, and preventing translation initiation complex from forma- tion. Conclusions Picornavirus inhibits host protein synthesisthe under the effect of virus nonstructural proteins.
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