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宿主因子TRIM5α和亲环素A对HIV-1复制的固有免疫作用。

The innate immune roles of host factors TRIM5α and Cyclophilin A on HIV-1 replication.

作者信息

Kuang Yi-Qun, Liu Hong-Liang, Zheng Yong-Tang

机构信息

Center for Translational Medicine, Huaihe Clinical Institute, Henan University, Kaifeng, 475004, Henan, People's Republic of China.

出版信息

Med Microbiol Immunol. 2015 Oct;204(5):557-65. doi: 10.1007/s00430-015-0417-y. Epub 2015 Apr 19.

Abstract

During the long-term evolutionary history, the interaction between virus and host has driven the first-line barrier, innate immunity, to invading pathogens. Innate immune factor TRIM5α and host peptidyl-prolyl cis-trans isomerase Cyclophilin A are two key players in the interaction between HIV-1 and host. Interestingly, Cyclophilin A is retrotransposed into the critical host gene, TRIM5, locus via LINE-1 element in some primate species including New World monkeys and Old World monkeys. This review aims to comprehensively discuss the sensing and immune activation procedures of TRIM5α innate signaling pathway through Cyclophilin A. It will then present the production of TRIMCyp chimeric gene and the different fusion patterns in primates. Finally, it will summarize the distinct restriction activity of TRIMCyp from different primates and explain the current understanding on the innate immune mechanisms involved in the early phase of the viral life cycle during HIV-1 replication.

摘要

在长期的进化历史中,病毒与宿主之间的相互作用促使一线屏障——固有免疫对入侵病原体产生反应。固有免疫因子TRIM5α和宿主肽基脯氨酰顺反异构酶亲环素A是HIV-1与宿主相互作用中的两个关键参与者。有趣的是,在包括新大陆猴和旧大陆猴在内的一些灵长类物种中,亲环素A通过LINE-1元件反转录转座到关键的宿主基因TRIM5位点。本综述旨在全面讨论通过亲环素A的TRIM5α固有信号通路的传感和免疫激活过程。然后将介绍TRIMCyp嵌合基因的产生以及灵长类动物中的不同融合模式。最后,将总结来自不同灵长类动物的TRIMCyp的不同限制活性,并解释目前对HIV-1复制过程中病毒生命周期早期所涉及的固有免疫机制的理解。

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