Regulation of MAVS Expression and Signaling Function in the Antiviral Innate Immune Response

Viral infection is controlled by host innate immune cells that express specialized receptors for viral components. Engagement of these pattern recognition receptors triggers a series of signaling pathways that culminate in the production of antiviral mediators such as type I interferons. Mitochondri...

Full description

Saved in:
Bibliographic Details
Published in:Frontiers in immunology 2020-05, Vol.11, p.1030-1030
Main Authors: Ren, Zhihua, Ding, Ting, Zuo, Zhicai, Xu, Zhiwen, Deng, Junliang, Wei, Zhanyong
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing - chemistry
Adaptor Proteins, Signal Transducing - genetics
Adaptor Proteins, Signal Transducing - immunology
Animals
Apoptosis - immunology
Autophagy - immunology
DEAD Box Protein 58 - metabolism
Host Microbial Interactions - genetics
Host Microbial Interactions - immunology
Humans
Immune Evasion
Immunity, Innate - genetics
Immunology
innate immunity
MAVS
Models, Immunological
molecular regulation
Protein Processing, Post-Translational
Receptors, Immunologic - metabolism
RNA Processing, Post-Transcriptional
Signal Transduction - immunology
Viral Proteins - immunology
viral replication
Virus Diseases - genetics
Virus Diseases - immunology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Viral infection is controlled by host innate immune cells that express specialized receptors for viral components. Engagement of these pattern recognition receptors triggers a series of signaling pathways that culminate in the production of antiviral mediators such as type I interferons. Mitochondrial antiviral-signaling protein (MAVS) acts as a central hub for signal transduction initiated by RIG-I-like receptors, which predominantly recognize viral RNA. MAVS expression and function are regulated by both post-transcriptional and post-translational mechanisms, of which ubiquitination and phosphorylation play the most important roles in modulating MAVS function. Increasing evidence indicates that viruses can escape the host antiviral response by interfering at multiple points in the MAVS signaling pathways, thereby maintaining viral survival and replication. This review summarizes recent studies on the mechanisms by which MAVS expression and signaling are normally regulated and on the various strategies employed by viruses to antagonize MAVS activity, which may provide new insights into the design of novel antiviral agents.
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2020.01030