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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
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Autophagy activated by duck enteritis virus infection positively affects its replication
Hai-Chang Yin1, Li-Li Zhao1, Si-Qi Li2
1State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agriculture Sciences, 678 Haping Road, Harbin 150069, PR China.
The Journal of General Virology
|December 24, 2016
Summary
Duck enteritis virus (DEV) infection triggers host cell autophagy, a process that enhances viral replication. Inhibiting autophagy reduces DEV, while inducing it increases viral yield, indicating autophagy facilitates DEV propagation.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Duck enteritis virus (DEV) causes a significant disease in poultry.
- Autophagy, a cellular degradation process, plays a role in various viral infections.
- The interaction between DEV and host cell autophagy remains poorly understood.
Purpose of the Study:
- To investigate whether DEV infection induces autophagy in duck cells.
- To determine the role of autophagy in DEV replication.
Main Methods:
- DEV infection of duck embryo fibroblast (DEF) cells.
- Microscopic observation of autophagosome formation and GFP-LC3 puncta.
- Western blot analysis of autophagy markers (LC3-I/II, p62/SQSTM1).
- Pharmacological inhibition (LY294002, wortmannin) and induction (rapamycin) of autophagy.
- Gene silencing of autophagy-related genes (Beclin-1, ATG5) using siRNA.
Main Results:
- DEV infection induced autophagosome formation and complete autophagy flux in DEF cells.
- Autophagy induction was dependent on DEV replication, as heat-inactivated DEV did not trigger it.
- Inhibition of autophagy decreased DEV replication, while autophagy induction enhanced it.
- Silencing Beclin-1 or ATG5 reduced DEV yield.
Conclusions:
- DEV infection activates autophagy in duck host cells.
- Autophagy facilitates DEV replication, suggesting it is a pro-viral mechanism.
- Targeting autophagy could be a potential strategy for controlling DEV infections.

