MAVS Human

Mitochondrial Antiviral Signaling Protein (MAVS), also known as CARDIF, IPS-1, and VISA, is a crucial component of the innate immune response against viral infections. MAVS is located on the outer membrane of mitochondria, peroxisomes, and the mitochondrial-associated endoplasmic reticulum membrane (MAM). It plays a pivotal role in the detection and response to viral pathogens, particularly RNA viruses .

MAVS is a protein encoded by the MAVS gene, which is located on chromosome 20 in humans. The protein contains a caspase activation and recruitment domain (CARD) that is essential for its function in antiviral signaling. Upon viral infection, MAVS acts as a central hub for signal transduction initiated by RIG-I-like receptors (RLRs), which predominantly recognize viral RNA .

When a virus infects a cell, viral RNA is detected by RLRs such as RIG-I and MDA5. These receptors then interact with MAVS through their CARD domains, leading to the formation of prion-like aggregates of MAVS. This aggregation is crucial for the activation of downstream signaling pathways that result in the production of type I interferons and other antiviral cytokines .

The expression and function of MAVS are tightly regulated by various post-transcriptional and post-translational mechanisms, including ubiquitination and phosphorylation. These modifications can either enhance or inhibit MAVS activity, thereby modulating the antiviral response. Viruses have evolved strategies to interfere with MAVS signaling, allowing them to evade the host immune response .

MAVS is essential for the host’s defense against a wide range of RNA viruses, including influenza, hepatitis C, and SARS-CoV-2. Dysregulation of MAVS signaling can lead to impaired immune responses and increased susceptibility to viral infections. Understanding the mechanisms of MAVS regulation and function can provide insights into the development of novel antiviral therapies .