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Virology. 2019 Nov;537:254-263. doi: 10.1016/j.virol.2019.08.029. Epub 2019 Aug 30.

Seneca valley virus activates autophagy through the PERK and ATF6 UPR pathways.

Author information

1
Beijing Key Laboratory for Prevention and Control of Infectious Diseases in Livestock and Poultry, Institute of Animal Husbandry and Veterinary Medicine, Beijing Academy of Agriculture and Forestry Sciences, Beijing, 100097, China.
2
College of Animal Husbandry and Veterinary Medicine, Xinyang Agriculture and Forestry University, Xinyang, 464000, China.
3
Beijing Key Laboratory for Prevention and Control of Infectious Diseases in Livestock and Poultry, Institute of Animal Husbandry and Veterinary Medicine, Beijing Academy of Agriculture and Forestry Sciences, Beijing, 100097, China. Electronic address: liujue@263.net.

Abstract

Diverse effects on autophagy, a cell degradation pathway, have been associated with the infectious mechanisms of different pathogens. Here, we demonstrated that Seneca valley virus (SVV), an important emerging porcine virus characterized by vesicular lesions and neonatal mortality, can induce autophagy in cultured PK-15 and BHK-21 cells by detecting autophagosome formation, GFP-LC3 puncta and accumulation of LC3-II proteins. Treatment with pharmacological inducers/inhibitors and small interfering RNA sequences targeting genes critical for autophagosome formation affected autophagy induction and viral yields. SVV induced a complete autophagic process to enhance its replication. The PERK and ATF6 pathways, two components of the endoplasmic reticulum (ER)-related unfolded protein response (UPR), were also activated in SVV-infected cells and downregulation of their expression suppressed SVV-induced autophagy and viral yields. Overall, these results reveal that SVV induces autophagy in cultured cells through the PERK and ATF6 pathways, thereby contributing to understanding of the molecular mechanisms underlying SVV pathogenesis.

KEYWORDS:

ATF6; Autophagy; PERK; Seneca valley virus; Viral replication

PMID:
31539773
DOI:
10.1016/j.virol.2019.08.029
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