Suppr超能文献

MX动力蛋白、寡腺苷酸合成酶和蛋白激酶R对1型干扰素体外抗副粘病毒活性的作用。

Contribution of MX dynamin, oligoadenylate synthetase, and protein kinase R to anti-paramyxovirus activity of type 1 interferons in vitro.

作者信息

Leroy Michaël P-P, Baise Etienne A, Pire Grégory A, Desmecht Daniel J-M

机构信息

Department of Pathology, Faculty of Veterinary Medicine, University of Liège, B-4000 Liège, Belgium.

出版信息

Am J Vet Res. 2007 Sep;68(9):988-94. doi: 10.2460/ajvr.68.9.988.

Abstract

OBJECTIVE

To determine the contribution of MX dynamin, oligoadenylate synthetase (OAS), and double-stranded RNA-dependent protein kinase R (PKR) to the antiviral effects of type 1 interferons (IFNs) against bovine parainfluenza-3 virus (PI-3V) infection of Vero cells.

SAMPLE POPULATION

Vero cell cultures.

PROCEDURES

PI-3V yield was first compared between control and transfected type 1 IFNs-incompetent Vero cells expressing recombinant OAS or MX proteins. Afterwards, phosphorylation of eukaryotic initiation factor 2 alpha (eIF2alpha) was used to scale the degree of PKR activation upon infection of Vero cells by PI-3V.

RESULTS

Overexpression of OAS did not result in significantly decreased viral replication. Phosphorylated eIF2alpha forms, the hallmark of PKR activation, were not increased in IFNalpha-primed infected Vero cells. Although human MXA contributed to partial blockade of replication of bovine PI-3V, the antiviral effect was not as strong as that of IFNalpha.

CONCLUSIONS AND CLINICAL RELEVANCE

The powerful anti-Paramyxovirus activity of type 1 IFNs is mediated by noncanonic pathways.

摘要

目的

确定MX发动蛋白、寡腺苷酸合成酶(OAS)和双链RNA依赖性蛋白激酶R(PKR)在1型干扰素(IFN)对牛副流感3型病毒(PI-3V)感染Vero细胞的抗病毒作用中的贡献。

样本群体

Vero细胞培养物。

实验步骤

首先比较对照Vero细胞与转染表达重组OAS或MX蛋白的无1型IFN能力的Vero细胞之间的PI-3V产量。之后,利用真核起始因子2α(eIF2α)的磷酸化来衡量PI-3V感染Vero细胞后PKR的激活程度。

结果

OAS的过表达并未导致病毒复制显著减少。PKR激活的标志——磷酸化eIF2α形式,在IFNα预处理的感染Vero细胞中并未增加。虽然人MXA有助于部分阻断牛PI-3V的复制,但抗病毒效果不如IFNα强。

结论及临床意义

1型IFN强大的抗副粘病毒活性由非经典途径介导。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验