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Mx Is Not Responsible for the Antiviral Activity of Interferon-α against Japanese Encephalitis Virus

Key Laboratory of Animal Diseases Diagnosis and Immunology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China
Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai 200241, China
Author to whom correspondence should be addressed.
Academic Editor: Michael R. Holbrook
Viruses 2017, 9(1), 5;
Received: 6 November 2016 / Revised: 14 December 2016 / Accepted: 28 December 2016 / Published: 10 January 2017
(This article belongs to the Special Issue Advances in Flavivirus Research)
PDF [9150 KB, uploaded 10 January 2017]


Mx proteins are interferon (IFN)-induced dynamin-like GTPases that are present in all vertebrates and inhibit the replication of myriad viruses. However, the role Mx proteins play in IFN-mediated suppression of Japanese encephalitis virus (JEV) infection is unknown. In this study, we set out to investigate the effects of Mx1 and Mx2 expression on the interferon-α (IFNα) restriction of JEV replication. To evaluate whether the inhibitory activity of IFNα on JEV is dependent on Mx1 or Mx2, we knocked down Mx1 or Mx2 with siRNA in IFNα-treated PK-15 cells and BHK-21 cells, then challenged them with JEV; the production of progeny virus was assessed by plaque assay, RT-qPCR, and Western blotting. Our results demonstrated that depletion of Mx1 or Mx2 did not affect JEV restriction imposed by IFNα, although these two proteins were knocked down 66% and 79%, respectively. Accordingly, expression of exogenous Mx1 or Mx2 did not change the inhibitory activity of IFNα to JEV. In addition, even though virus-induced membranes were damaged by Brefeldin A (BFA), overexpressing porcine Mx1 or Mx2 did not inhibit JEV proliferation. We found that BFA inhibited JEV replication, not maturation, suggesting that BFA could be developed into a novel antiviral reagent. Collectively, our findings demonstrate that IFNα inhibits JEV infection by Mx-independent pathways. View Full-Text
Keywords: Mx1; Mx2; interferon-α (IFNα); Japanese encephalitis virus (JEV); antivirus; Brefeldin A (BFA) Mx1; Mx2; interferon-α (IFNα); Japanese encephalitis virus (JEV); antivirus; Brefeldin A (BFA)

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Zhou, J.; Wang, S.-Q.; Wei, J.-C.; Zhang, X.-M.; Gao, Z.-C.; Liu, K.; Ma, Z.-Y.; Chen, P.-Y.; Zhou, B. Mx Is Not Responsible for the Antiviral Activity of Interferon-α against Japanese Encephalitis Virus. Viruses 2017, 9, 5.

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