Abstract
Mitochondrial antiviral signaling protein (MAVS) functions as a “switch” in the immune signal transduction against most RNA viruses. Upon viral infection, MAVS forms prion-like aggregates by receiving the cytosolic RNA sensor retinoic acid-inducible gene I-activated signaling and further activates/switches on the type I interferon signaling. While under resting state, MAVS is prevented from spontaneously aggregating to switch off the signal transduction and maintain immune homeostasis. Due to the dual role in antiviral signal transduction and immune homeostasis, MAVS has emerged as the central regulation target by both viruses and hosts. Recently, researchers show increasing interest in viral evasion strategies and immune homeostasis regulations targeting MAVS, especially focusing on the post-translational modifications of MAVS, such as ubiquitination and phosphorylation. This review summarizes the regulations of MAVS in antiviral innate immune signaling transduction and immune homeostasis maintenance.
Highlights
The battle between humans and viruses is never ending
Induces Mitochondrial antiviral signaling protein (MAVS) lysosomal autophagy with the help of NDP52 (Jin et al, 2017; Jin and Cui, 2018) Promotes the autophagy degradation of MAVS aggregates (He et al, 2019) c-Abl positively regulates RLR signaling by phosphorylating MAVS (Cheng et al, 2016) TBK1 and IKKbβ directly phosphorylate MAVS and recruit IRF3 for its phosphorylation by TBK1 (Liu et al, 2015) NAC1 takes bridge effect between MAVS and TBK1 (Xia et al, 2019) Nemo-like kinase (NLK) phosphorylate and degrade MAVS by associating with MAVS (Li et al, 2019a) PPM1A directly dephosphorylates the phosphorylated MAVS induced by TBK1 PLK1 phosphorylates the central T234 residue of MAVS (Vitour et al, 2009)
MAVS acts as an adaptor in RNA-sensing signaling pathways to induce IFN production by forming prion-like aggregates after receiving upstream signals from pattern recognition receptors (PRRs)
Summary
The battle between humans and viruses is never ending. New emerging viruses, such as SARS-CoV-2 ( referred to as 2019-nCoV), pose a tremendous threat to public health. Innate immunity is the body’s first line of defense against foreign pathogens. It consists of tissue barriers (skin and mucous membranes), phagocytes (macrophages and neutrophils), dendritic cells (DC), and killer cells (Thompson and Locarnini, 2007). Innate immunity produces interferons (IFNs) and pro-inflammatory factors to inhibit and eliminate the invading pathogens and maintain the hots immune homeostasis. IFNs have immunomodulatory effects and can activate acquired immunity through antigen presentation. Innate immunity plays a key role in inhibiting tumor growth and metastasis
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