文献类型：期刊文献

中文题名：HIV-1始祖病毒Vpu和Vif拮抗宿主限制因子的能力

英文题名：Abilities of HIV-1 founder virus Vpu and Vif to counteract host restriction factor

作者：黄宇明[1];赵建元[2];岑山[2];魏涛[3]

第一作者：黄宇明

机构：[1]首都医科大学附属北京地坛医院;[2]中国医学科学院北京协和医学院医药生物技术研究所;[3]北京联合大学生物化学工程学院

第一机构：首都医科大学附属北京地坛医院,北京100015

年份：2017

卷号：12

期号：4

起止页码：303-309

中文期刊名：中国医药生物技术

外文期刊名：Chinese Medicinal Biotechnology

收录：CSTPCD

基金：国家自然科学基金(31470076;31470272);国家重大科学研究计划(2012CB911102)

语种：中文

中文关键词：vpu基因产物,人免疫缺陷病毒;vif基因产物,人免疫缺陷病毒;HIV-1始祖病毒

外文关键词：vpu gene products, human immunodeficiency virus; vifgene products, human immunodeficiency virus; HIV-1 founder virus

摘要：目的研究始祖病毒的生物学和早期进化特征,有助于阐明HIV-1建立感染的关键因素。方法以过表达的方法比较了始祖病毒和同一亚型的慢性感染病毒Vpu蛋白降解宿主限制因子BST-2的能力,利用流式细胞术检测两者对内源性BST-2细胞表面水平的影响。利用已构建的含荧光素酶报告基因的单循环感染始祖病毒表达质粒,比较了始祖病毒与同一亚型的慢性感染株下调BST-2的能力。用过表达的方法检测了Vif蛋白拮抗宿主限制因子h A3G的能力。结果对过表达以及细胞表面内源性BST-2,始祖病毒Vpu蛋白降解宿主限制因子BST-2的能力均显著高于同一亚型的慢性感染病毒。但在始祖病毒拮抗BST-2抗病毒活性的能力分析中,尽管始祖病毒Vpu表现出较强的下调BST-2的能力,仍然不足以拮抗外源过量表达的BST-2的抗病毒活性。在Vif降解hA 3G的实验中,始祖病毒Vif降解h A3G的能力弱于慢性感染病毒p MJ4或与之类似。结论始祖病毒具有更高的拮抗宿主天然免疫的能力,有助于其建立早期感染。
Objective To study the biology and early evolutionary characteristics of founder virus for better understanding of the key factors involved in establishment of new infection. Methods With the methods of over-expression, we compared the ability of Vpu protein from transimitted/founder （T/F） virus and chronic strain to counteract host restriction factors BST-2 and the effect on endogenous BST-2 on the cell surface by flow cytometer. Using the constructed single-cycle infectious virus within luciferase reporter gene, we compared the ability of down-regulation of BST-2 in T/F virus and chronic virus. The ability of the Vifprotein to antagonize the host restriction factor hA3G was also examined by overexpression. Results The results showed that Vpu of T/F virus exhibited significantly improved ability to reduce the level of BST-2, as compared with that of chronic strain, while no difference in the Vif-mediated hA3G degradation was observed. Conclusion T/F virus may possess better ability to counteract with host innate immunity to facilitate the establishment of new infection.