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Vet Res. 2019 Feb 28;50(1):16. doi: 10.1186/s13567-019-0636-0.

14-3-3ε acts as a proviral factor in highly pathogenic porcine reproductive and respiratory syndrome virus infection.

Cao S1,2,3, Cong F1,2,3, Tan M1,2,3, Ding G1,2,3, Liu J1,2,3, Li L1,2,3, Zhao Y1,2,3, Liu S1,2,3, Xiao Y4,5,6.

Author information

1
Department of Fundamental Veterinary Medicine, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai'an, China.
2
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, Tai'an, China.
3
Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Shandong Agricultural University, Tai'an, China.
4
Department of Fundamental Veterinary Medicine, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai'an, China. xiaoyihong01@163.com.
5
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, Tai'an, China. xiaoyihong01@163.com.
6
Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Shandong Agricultural University, Tai'an, China. xiaoyihong01@163.com.

Abstract

The highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) emerged in 2006 in China and caused great economic losses for the swine industry because of the lack of an effective vaccine. 14-3-3 proteins are generating significant interest as potential drug targets by allowing the targeting of specific pathways to elicit therapeutic effects in human diseases. In a previous study, 14-3-3s were identified to interact with non-structural protein 2 (NSP2) of PRRSV. In the present study, the specific subtype 14-3-3ε was confirmed to interact with NSP2 and play a role in the replication of the HP-PRRSV TA-12 strain. Knockdown of 14-3-3ε in Marc-145 cells and porcine alveolar macrophages (PAMs) caused a significant decrease in TA-12 replication, while stable overexpression of 14-3-3ε caused a significant increase in the replication of TA-12 and low pathogenic PRRSV (LP-PRRSV) CH-1R. The 14-3-3 inhibitor difopein also decreased TA-12 and CH-1R replication in Marc-145 cells and PAMs. These findings are consistent with 14-3-3ε acting as a proviral factor and suggest that 14-3-3ε siRNA and difopein are therapeutic candidates against PRRSV infection.

PMID:
30819256
PMCID:
PMC6394020
DOI:
10.1186/s13567-019-0636-0
[Indexed for MEDLINE]
Free PMC Article

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