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

ABSTRACT: 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-? (IFN?) restriction of JEV replication. To evaluate whether the inhibitory activity of IFN? on JEV is dependent on Mx1 or Mx2, we knocked down Mx1 or Mx2 with siRNA in IFN?-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 IFN?, 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 IFN? 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 IFN? inhibits JEV infection by Mx-independent pathways.

SUBMITTER: Zhou J 

PROVIDER: S-EPMC5294974 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature