Abstract
Hepatitis E virus (HEV) infection is the leading cause of acute hepatitis worldwide. Mitochondrial antiviral signaling protein (MAVS)-mediated interferon (IFN) response plays a pivotal role in the hepatic antiviral immunity. However, little is known about the effects of overexpression of MAVS on HEV infection. Here, we studied the effects of FL-MAVS on HEV. We found that overexpression of FL-MAVS profoundly inhibited HEV replication. The overexpression of FL-MAVS is accompanied by the secretion of functional IFNs and transcriptional induction of interferon stimulated genes (ISGs). Furthermore, we showed that the anti-HEV effect of FL-MAVS is largely dependent of the JAK signaling activation.