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Published in: Virology Journal 1/2014

Open Access 01-12-2014 | Research

Nonstructural proteins 2C and 3D are involved in autophagy as induced by the encephalomyocarditis virus

Authors: Lei Hou, Xinna Ge, Lingxiang Xin, Lei Zhou, Xin Guo, Hanchun Yang

Published in: Virology Journal | Issue 1/2014

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Abstract

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.
Appendix
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Metadata
Title
Nonstructural proteins 2C and 3D are involved in autophagy as induced by the encephalomyocarditis virus
Authors
Lei Hou
Xinna Ge
Lingxiang Xin
Lei Zhou
Xin Guo
Hanchun Yang
Publication date
01-12-2014
Publisher
BioMed Central
Published in
Virology Journal / Issue 1/2014
Electronic ISSN: 1743-422X
DOI
https://doi.org/10.1186/1743-422X-11-156

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