E3 ubiquitin ligase RNF114 promotes vesicular stomatitis virus replication via inhibiting type I interferon production

Abstract

As a single-stranded RNA virus, vesicular stomatitis virus (VSV) causes influenza-like clinical symptoms in infected individuals. Type-I interferon signaling pathway plays a vital role in inhibiting VSV replication. It has been shown that RNF114 (RING finger protein 114) acts as an E3 ubiquitin ligase to regulate the type-I interferon signaling pathway. In contrast, the effects of RNF114 from Chinese sturgeon or sea perch remain controversial. In the present study, we reported the effect of human RNF114 on VSV infection. Overexpression of RNF114 promoted VSV replication, while depletion of RNF114 reduced viral replication. We further found that RNF114 inhibited type-I interferon production via interacting with mitochondrial antiviral signaling protein (MAVS). Moreover, in vivo experiments demonstrated that RNF114 could also accelerate VSV replication and virus-induced inflammation in lung tissues. Collectively, our findings supported that RNF114 negatively regulated the type-I interferon signaling pathway during VSV replication, providing novel and favorable insights into clinical treatment of VSV infection.