β-干扰素通过一种依赖于RNase L的途径抑制三叉神经节细胞中的单纯疱疹病毒1型复制。
Interferon-beta suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway.
作者信息
Carr Daniel J J, Al-khatib Khaldun, James Cassandra M, Silverman Robert
机构信息
Department of Ophthalmology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
出版信息
J Neuroimmunol. 2003 Aug;141(1-2):40-6. doi: 10.1016/s0165-5728(03)00216-9.
Abstract
The induction of an antiviral state by type I interferons (IFN) was evaluated in primary trigeminal ganglion cell cultures using herpes simplex virus type 1 (HSV-1). Cells treated with mouse IFN-beta consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-alpha1, IFN-alpha4, IFN-alpha5, IFN-alpha6, or IFN-alpha9. The antiviral efficacy was dose-dependent and correlated with the induction of the IFN-inducible, antiviral genes, 2'-5' oligoadenylate synthetase (OAS) and double-stranded RNA-dependent protein kinase. In trigeminal ganglion cells deficient in the downstream effector molecule of the OAS pathway, RNase L, the antiviral state induced by IFN-beta was lost.
摘要
使用1型单纯疱疹病毒（HSV-1）在原代三叉神经节细胞培养物中评估了I型干扰素（IFN）诱导抗病毒状态的能力。与用IFN-α1、IFN-α4、IFN-α5、IFN-α6或IFN-α9处理的细胞相比，用小鼠IFN-β处理的细胞始终表现出对HSV-1感染的最强抗性。抗病毒效力呈剂量依赖性，并且与IFN诱导的抗病毒基因2'-5'寡腺苷酸合成酶（OAS）和双链RNA依赖性蛋白激酶的诱导相关。在OAS途径的下游效应分子核糖核酸酶L缺陷的三叉神经节细胞中，IFN-β诱导的抗病毒状态丧失。
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