Mitochondrial antiviral-signaling protein

Definition:

Required for innate immune defense against viruses. Acts downstream of DHX33, RIGI and IFIH1/MDA5, which detect intracellular dsRNA produced during viral replication, to coordinate pathways leading to the activation of NF-kappa-B, IRF3 and IRF7, and to the subsequent induction of antiviral cytokines such as IFNB and RANTES (CCL5). Peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state. Upon viral infection, peroxisomal MAVS induces the rapid interferon-independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon-dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response. May activate the same pathways following detection of extracellular dsRNA by TLR3. May protect cells from apoptosis.

References:

[1]. Evelyn Dixit, et al. Peroxisomes are signaling platforms for antiviral innate immunity. Cell. 2010 May 14;141(4):668-81. [Content Brief]

[2]. Xin-Yi Liu, et al. Tom70 mediates activation of interferon regulatory factor 3 on mitochondria. Cell Res. 2010 Sep;20(9):994-1011. [Content Brief]

[3]. Liang-Guo Xu, et al. VISA is an adapter protein required for virus-triggered IFN-beta signaling. Mol Cell. 2005 Sep 16;19(6):727-40. [Content Brief]

[4]. Taro Kawai, et al. IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction. Nat Immunol. 2005 Oct;6(10):981-8. [Content Brief]

[5]. Yu-Hsin Chiu, et al. RNA polymerase III detects cytosolic DNA and induces type I interferons through the RIG-I pathway. Cell. 2009 Aug 7;138(3):576-91. [Content Brief]

[6]. Yu-Zhi Fu, et al. SARS-CoV-2 membrane glycoprotein M antagonizes the MAVS-mediated innate antiviral response. Cell Mol Immunol. 2021 Mar;18(3):613-620. [Content Brief]

[7]. Siqi Liu, et al. Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation. Science. 2015 Mar 13;347(6227):aaa2630. [Content Brief]

[8]. Etienne Meylan, et al. Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus. Nature. 2005 Oct 20;437(7062):1167-72. [Content Brief]

[9]. Hiroyuki Oshiumi, et al. DEAD/H BOX 3 (DDX3) helicase binds the RIG-I adaptor IPS-1 to up-regulate IFN-beta-inducing potential. Eur J Immunol. 2010 Apr;40(4):940-8. [Content Brief]

[10]. Hiroyuki Oshiumi, et al. Hepatitis C virus core protein abrogates the DDX3 function that enhances IPS-1-mediated IFN-beta induction. PLoS One. 2010 Dec 8;5(12):e14258. [Content Brief]

[11]. Yetao Wang, et al. Ndfip1 negatively regulates RIG-I-dependent immune signaling by enhancing E3 ligase Smurf1-mediated MAVS degradation. J Immunol. 2012 Dec 1;189(11):5304-13. [Content Brief]

[12]. Rashu B Seth, et al. Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-kappaB and IRF 3. Cell. 2005 Sep 9;122(5):669-82. [Content Brief]

[13]. Young Bong Choi, et al. TAX1BP1 Restrains Virus-Induced Apoptosis by Facilitating Itch-Mediated Degradation of the Mitochondrial Adaptor MAVS. Mol Cell Biol. 2016 Dec 19;37(1):e00422-16. [Content Brief]

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