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MicroRNA-30a-5p promotes replication of porcine circovirus type 2 through enhancing autophagy by targeting 14-3-3

Authors
  • Wang, Xiaomin1, 2
  • Xu, Xianglan1, 2
  • Wang, Wei2
  • Yu, Zhengyu2
  • Wen, Libin2
  • He, Kongwang2, 3
  • Fan, Hongjie1, 3
  • 1 Nanjing Agricultural University, College of Veterinary Medicine, Nanjing, 210095, China , Nanjing (China)
  • 2 National Center for Engineering Research of Veterinary Bio-products, Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Key Laboratory of Veterinary Biological Engineering and Technology, Ministry of Agriculture, Nanjing, 210014, China , Nanjing (China)
  • 3 Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, China , Yangzhou (China)
Type
Published Article
Journal
Archives of Virology
Publisher
Springer-Verlag
Publication Date
May 22, 2017
Volume
162
Issue
9
Pages
2643–2654
Identifiers
DOI: 10.1007/s00705-017-3400-7
Source
Springer Nature
Keywords
License
Yellow

Abstract

Accumulating evidence demonstrates that autophagy and microRNAs (miRNAs) play key roles in regulating virus-host interactions and can restrict or facilitate viral replication. In the present study we examined whether a functional relationship exists between autophagy, miRNA and porcine circovirus type 2 (PCV2) infection, using several approaches. We demonstrated that there was a positive correlation between PCV2 infection and autophagy in 3D4/21 cells and autophagy induced by PCV2 infection triggered PCV2 replication. Four miRNA were selected by real-time PCR and further studied, but only miR-30a-5p mimic had a significant effect on PCV2 replication. Overexpression of miR-30a-5p significantly enhanced PCV2 infection and autophagy in a dose-dependent manner. Blockage of miR-30a-5p significantly decreased PCV2 replication. We provided further evidence that miR-30a-5p regulate the link between PCV2 infection and host immune system. Furthermore, miR-30a-5p targeted and regulated 14-3-3 gene, which is a regulator of autophagy. Flow cytometry data demonstrated that miR-30a-5p promotes cell cycle arrest at the G2 phase to regulate PCV2 replication and autophagy by interacting directly with 14-3-3, but not with the PCV2 genome. These data not only provide new insights into virus-host interactions during PCV2 infection but also suggest a potential new antiviral therapeutic strategy against PCV2 infection.

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