Nonstructural proteins 2C and 3D are involved in autophagy as induced by the encephalomyocarditis virus
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- 作者：Lei Hou (1)
Xinna Ge (1)
Lingxiang Xin (1)
Lei Zhou (1)
Xin Guo (1)
Hanchun Yang (1)
1. Key Laboratory of Animal Epidemiology and Zoonosis of the Ministry of Agriculture ; College of Veterinary Medicine and State Key Laboratory of Agrobiotechnology ; China Agricultural University ; No. 2 Yuanmingyuan West Road ; Haidian District ; Beijing ; 100193 ; People鈥檚 Republic of China - 关键词：Encephalomyocarditis virus (EMCV) ; Nonstructural protein ; 2C ; 3D ; Autophagy ; Endoplasmic reticulum (ER) stress ; Unfolded protein response (UPR)
- 刊名：Virology Journal
- 出版年：2014
- 出版时间：December 2014
- 年：2014
- 卷：11
- 期：1
- 全文大小：2,055 KB
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- 出版者：BioMed Central
- ISSN：1743-422X
文摘
Background Encephalomyocarditis virus (EMCV) can infect a variety of animal species and humans. Although the EMCV infection is known to induce autophagy to promote its replication in host cells, the viral proteins that are responsible for inducing autophagy are unknown. Methods The recombinant plasmids that were expressing the EMCV proteins were constructed to analyze the role of each protein in the induction of autophagy. Autophagy inductions by the EMCV proteins in BHK-21 cells were investigated by confocal microscopy, Western blotting and transmission electron microscopy. ER stress in BHK-21 cells was examined by detecting the marker molecules using western blotting and luciferase assays. Results This study presents the first demonstration that the nonstructural proteins 2C or 3D of EMCV were involved in inducing autophagy in BHK-21 cells that were expressing 2C or 3D, and we found that inhibiting Beclin1 expression influenced this autophagy induction process. Next, 2C and 3D were shown to be involved in inducing autophagy by activating the ER stress pathway. Finally, EMCV 2C or 3D were demonstrated to regulate the proteins associated with PERK and ATF6alpha pathway. Conclusions Our findings indicate that 2C and 3D are involved in EMCV-induced autophagy by activating ER stress molecules and regulating the proteins expression associated with UPR pathway, helping to better understand the EMCV-induced autophagy process.