E3 ubiquitin ligase RNF114 promotes vesicular stomatitis virus replication via inhibiting type I interferon production. (June 2022)

• Record Type: Journal Article
• Authors: Han, Wenzheng; Chen, Qing; Cui, Jun; Zhao, Yinxia; Li, Min; Li, Xiaoning
• Is Part Of: Microbial pathogenesis. Volume 167(2022)
• Publication Date: 2022-06
• Subjects: Vesicular stomatitis virus -- E3 ubiquitin ligase -- RNF114 -- Type-I interferon -- Inflammation; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2022.105569
• Languages: English
• ISSNs: 0882-4010

Abstract

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. Highlights: The expression of RNF114 is induced upon VSV infection. Overexpression of RNF114 promotes VSV replication in A549 cells. Knockdown of RNF114 suppresses VSV replication in A549 cells. RNF114 inhibits VSV-induced type-I IFN production via interacting with MAVS. The RING domain is required for the effect of RNF114 on VSV replication. Overexpression of RNF114 in vivo significantly promotes VSV replication and aggravates virus-induced inflammation in the lung.