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Updated: May 15, 2026
09:10
siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
Peste des petits ruminants virus exploits cellular autophagy machinery for replication
Yongning Zhang1, Shaoqiang Wu, Jizhou Lv
1Institute of Animal Quarantine, Chinese Academy of Inspection and Quarantine, Beijing 100029, People's Republic of China.
Virology
|January 16, 2013
Summary
Peste des petits ruminants virus (PPRV) hijacks host cell autophagy for replication. Enhancing autophagy boosts PPRV yield, suggesting therapeutic targets for vaccine production.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Peste des petits ruminants virus (PPRV) significantly impacts small ruminant productivity globally.
- PPRV is known to induce apoptosis, but its interaction with host cells, specifically regarding autophagy, needs further investigation.
Purpose of the Study:
- To investigate the role of autophagy in PPRV infection of permissive cells.
- To determine if PPRV utilizes the autophagy pathway for its replication.
Main Methods:
- Vero cells were infected with PPRV.
- Autophagy was assessed by electron microscopy, LC3 puncta analysis, and LC3-I/-II conversion.
- Autophagy was modulated using rapamycin (induction) and ATG7 siRNA (inhibition).
- PPRV progeny yield and N protein expression were quantified.
Main Results:
- PPRV infection triggered significant autophagy in Vero cells, evidenced by vesicle formation, LC3 accumulation, and enhanced autophagic flux.
- Autophagy induction via rapamycin increased PPRV yield and N protein levels.
- Autophagy inhibition using ATG7 siRNA decreased PPRV yield and N protein levels.
Conclusions:
- PPRV infection induces autophagy in host cells.
- PPRV exploits the autophagy machinery to enhance its replication.
- Targeting the autophagic pathway could improve the production efficiency of live attenuated PPRV vaccines.
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