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干扰素刺激基因:在病毒发病机制中的作用

Interferon-stimulated genes: roles in viral pathogenesis.

作者信息

Schoggins John W

机构信息

Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, United States.

出版信息

Curr Opin Virol. 2014 Jun;6:40-6. doi: 10.1016/j.coviro.2014.03.006. Epub 2014 Apr 5.

DOI:10.1016/j.coviro.2014.03.006
PMID:24713352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4077717/
Abstract

Interferon-stimulated genes (ISGs) are critical for controlling virus infections. As new antiviral ISGs continue to be identified and characterized, their roles in viral pathogenesis are also being explored in more detail. Our current understanding of how ISGs impact viral pathogenesis comes largely from studies in knockout mice, with isolated examples from human clinical data. This review outlines recent developments on the contributions of various ISGs to viral disease outcomes in vivo.

摘要

干扰素刺激基因(ISGs)对于控制病毒感染至关重要。随着新的抗病毒ISGs不断被鉴定和表征,它们在病毒发病机制中的作用也在更详细地探索中。我们目前对ISGs如何影响病毒发病机制的理解很大程度上来自基因敲除小鼠的研究,以及人类临床数据中的个别例子。本综述概述了各种ISGs对体内病毒疾病结果贡献的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c64/7102807/8b9f62ebdd0e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c64/7102807/8b9f62ebdd0e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c64/7102807/8b9f62ebdd0e/gr1.jpg

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Defining the range of pathogens susceptible to Ifitm3 restriction using a knockout mouse model.利用 knockout 小鼠模型定义易受 Ifitm3 限制的病原体范围。
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Ifit2 deficiency results in uncontrolled neurotropic coronavirus replication and enhanced encephalitis via impaired alpha/beta interferon induction in macrophages.
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