Mitochondrial antiviral-signaling protein (MAVS)

Mitochondrial antiviral-signaling protein (MAVS) is a critical adaptor protein located on the outer mitochondrial membrane, and also associated membranes such as peroxisomes and mitochondrial-associated ER membranes. It acts as a central hub in the innate immune response to viral infection, particularly for RNA viruses. Upon detecting cytosolic viral double-stranded RNA through sensors such as RIG-I and MDA5, MAVS becomes activated via CARD-CARD domain interactions, leading to the formation of self-perpetuating aggregates or filaments. MAVS then recruits downstream signaling proteins and scaffolds, inducing activation of kinases (IKKα, IKKβ, IKKγ/NEMO) and transcription factors (NF-κB, IRF3, IRF7), resulting in the production of type I interferons and inflammatory cytokines. MAVS function is tightly regulated by ubiquitination and phosphorylation, and viruses have evolved numerous countermeasures targeting MAVS to evade host immunity. While not a classical receptor or enzyme, MAVS is considered a therapeutic target for modulating antiviral immunity and is implicated in infection, inflammation, and autoimmunity. Direct pharmacological targeting is investigational and presents challenges related to specificity and immune regulation.

Other names

IPS-1VISAKIAA1271CardifIFN-β promoter stimulator 1Interferon beta promoter stimulator protein 1CARD adapter inducing interferon betaCARDIFVirus-induced-signaling adapterVirus-induced signaling adaptorPutative NF-kappa-B-activating protein 031N

Activation or inhibition of MAVS would modulate induction of type I interferons and other cytokines, influencing the downstream antiviral immune response