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中国农科院哈兽研发现猪传染性胃肠炎病毒感染可诱导靶细胞自噬

2018-07-26 来源:中国病毒学论坛  标签: 掌上医生 喝茶减肥 一天瘦一斤 安全减肥 cps联盟 美容护肤
摘要:猪传染性胃肠炎是由猪传染性胃肠炎病毒引起的一种以呕吐、严重腹泻和脱水性肠炎为主要特征的高度接触性、致死性传染病,是目前严重危害国内外养猪业的重要疫病之一。

 近日,从中国农业科学院哈尔滨兽医研究所传出喜讯,该所冯力研究员领衔的猪消化道传染病创新团队在研究中获得重要发现:猪传染性胃肠炎病毒感染可诱导靶细胞自噬,继而抑制病毒的复制。该研究结果发表在近期国际知名期刊《Scientific Reports》(科学通报)上,相关链接:http://www.ncbi.nlm.nih.gov/pubmed/27029407。

 
TGEV infection-induced autophagy is dependent of viral replication.
 
猪传染性胃肠炎是由猪传染性胃肠炎病毒引起的一种以呕吐、严重腹泻和脱水性肠炎为主要特征的高度接触性、致死性传染病,是目前严重危害国内外养猪业的重要疫病之一。猪传染性胃肠炎病毒为冠状病毒科的重要成员之一,该病毒主要感染哺乳仔猪,两周龄哺乳猪致死率高达100%,为养猪业带来严重的经济损失。
 
该团队王玉娥研究员、郭龙军博士发现猪传染性胃肠炎病毒感染能够诱导靶细胞自噬(机体降解有害物质的一种分解代谢过程)。药物处理诱导细胞自噬可抑制猪传染性胃肠炎病毒的感染复制;特异性抑制细胞自噬形成则可促进猪传染性胃肠炎病毒的感染复制。此外,研究人员还通过三维活细胞实时成像系统,获得猪传染性胃肠炎病毒感染后自噬体的发生、发展及降解等生物学变化过程。
 
据王玉娥研究员介绍,该研究为深入理解猪传染性胃肠炎病毒的致病机制提供理论基础,为合理防控该病毒病的发生和发展提供科学依据和新思路。
 
Sci Rep. 2016 Mar 31;6:23864. doi: 10.1038/srep23864.
 
Autophagy Negatively Regulates Transmissible Gastroenteritis Virus Replication.
 
Guo L1, Yu H1,2, Gu W1, Luo X1, Li R1, Zhang J1, Xu Y1, Yang L1, Shen N1, Feng L1, Wang Y1.
 
Abstract
 
Autophagy is an evolutionarily ancient pathway that has been shown to be important in the innate immune defense against several viruses. However, little is known about the regulatory role of autophagy in transmissible gastroenteritis virus (TGEV) replication. In this study, we found that TGEV infection increased the number of autophagosome-like double- and single-membrane vesicles in the cytoplasm of host cells, a phenomenon that is known to be related to autophagy. In addition, virus replication was required for the increased amount of the autophagosome marker protein LC3-II. Autophagic flux occurred in TGEV-infected cells, suggesting that TGEV infection triggered a complete autophagic response. When autophagy was pharmacologically inhibited by wortmannin or LY294002, TGEV replication increased. The increase in virus yield via autophagy inhibition was further confirmed by the use of siRNA duplexes, through which three proteins required for autophagy were depleted. Furthermore, TGEV replication was inhibited when autophagy was activated by rapamycin. The antiviral response of autophagy was confirmed by using siRNA to reduce the expression of gene p300, which otherwise inhibits autophagy. Together, the results indicate that TGEV infection activates autophagy and that autophagy then inhibits further TGEV replication.
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