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本文引用的文献

1
STING Requires the Adaptor TRIF to Trigger Innate Immune Responses to Microbial Infection.STING需要衔接蛋白TRIF来触发对微生物感染的先天免疫反应。
Cell Host Microbe. 2016 Sep 14;20(3):329-341. doi: 10.1016/j.chom.2016.08.002.
2
Relative Contributions of Herpes Simplex Virus 1 ICP0 and vhs to Loss of Cellular IFI16 Vary in Different Human Cell Types.单纯疱疹病毒1型ICP0和vhs对细胞IFI16缺失的相对贡献在不同人类细胞类型中有所不同。
J Virol. 2016 Aug 26;90(18):8351-9. doi: 10.1128/JVI.00939-16. Print 2016 Sep 15.
3
Interferons and inflammasomes: Cooperation and counterregulation in disease.干扰素和炎症小体:疾病中的合作与负调控。
J Allergy Clin Immunol. 2016 Jul;138(1):37-46. doi: 10.1016/j.jaci.2016.05.010. Epub 2016 May 24.
4
Viral Spread to Enteric Neurons Links Genital HSV-1 Infection to Toxic Megacolon and Lethality.病毒传播至肠神经元将生殖器单纯疱疹病毒1型感染与中毒性巨结肠及致死性联系起来。
Cell Host Microbe. 2016 Jun 8;19(6):788-99. doi: 10.1016/j.chom.2016.05.008.
5
HSV-1 ICP27 targets the TBK1-activated STING signalsome to inhibit virus-induced type I IFN expression.单纯疱疹病毒1型的ICP27靶向TBK1激活的STING信号小体,以抑制病毒诱导的I型干扰素表达。
EMBO J. 2016 Jul 1;35(13):1385-99. doi: 10.15252/embj.201593458. Epub 2016 May 27.
6
Human TBK1: A Gatekeeper of Neuroinflammation.人类TBK1:神经炎症的守护者。
Trends Mol Med. 2016 Jun;22(6):511-527. doi: 10.1016/j.molmed.2016.04.006.
7
PML plays both inimical and beneficial roles in HSV-1 replication.早幼粒细胞白血病蛋白在单纯疱疹病毒1型复制中发挥着有害和有益的双重作用。
Proc Natl Acad Sci U S A. 2016 May 24;113(21):E3022-8. doi: 10.1073/pnas.1605513113. Epub 2016 May 9.
8
Innate defense mechanisms against HSV-1 infection in the target tissues, skin and brain.针对单纯疱疹病毒1型(HSV-1)感染,在靶组织皮肤和大脑中的固有防御机制。
J Neurovirol. 2016 Oct;22(5):641-649. doi: 10.1007/s13365-016-0440-9. Epub 2016 Apr 20.
9
Programmed necrosis in inflammation: Toward identification of the effector molecules.程序性细胞坏死与炎症:寻找效应分子。
Science. 2016 Apr 1;352(6281):aaf2154. doi: 10.1126/science.aaf2154.
10
Evasion of host antiviral innate immunity by HSV-1, an update.单纯疱疹病毒1型对宿主抗病毒天然免疫的逃避:最新进展
Virol J. 2016 Mar 8;13:38. doi: 10.1186/s12985-016-0495-5.

固有免疫机制与单纯疱疹病毒感染及疾病

Innate Immune Mechanisms and Herpes Simplex Virus Infection and Disease.

作者信息

Kurt-Jones Evelyn A, Orzalli Megan H, Knipe David M

机构信息

Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, 01605, USA.

Division of Gastroenterology, Boston Children's Hospital, Boston, MA, 02115, USA.

出版信息

Adv Anat Embryol Cell Biol. 2017;223:49-75. doi: 10.1007/978-3-319-53168-7_3.

DOI:10.1007/978-3-319-53168-7_3
PMID:28528439
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7254490/
Abstract

Innate immune responses play a major role in the control of herpes simplex virus (HSV) infections, and a multiplicity of mechanisms have emerged as a result of human evolution to sense and respond to HSV infections. HSV in turn has evolved a number of ways to evade immune detection and to blunt human innate immune responses. In this review, we summarize the major host innate immune mechanisms and the HSV evasion mechanisms that have evolved. We further discuss how disease can result if this equilibrium between virus and host response is disrupted.

摘要

先天免疫反应在单纯疱疹病毒(HSV)感染的控制中起主要作用,由于人类进化,出现了多种感知和应对HSV感染的机制。反过来,HSV也进化出了多种逃避免疫检测和削弱人类先天免疫反应的方法。在这篇综述中,我们总结了主要的宿主先天免疫机制以及已进化出的HSV逃避机制。我们还进一步讨论了如果病毒与宿主反应之间的这种平衡被打破会如何导致疾病。