SARS‐CoV‐2 modulation of RIG‐I‐MAVS signaling: Potential mechanisms of impairment on host antiviral immunity and therapeutic approaches

The coronavirus disease 2019 (COVID‐19) is a global infectious disease aroused by RNA virus severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). Patients may suffer from severe respiratory failure or even die, posing a huge challenge to global public health. Retinoic acid‐inducible gene I (RIG‐I) is one of the major pattern recognition receptors, function to recognize RNA viruses and mediate the innate immune response. RIG‐1 and melanoma differentiation‐associated gene 5 contain an N‐terminal caspase recruitment domain that is activated upon detection of viral RNA in the cytoplasm of virus‐infected cells. Activated RIG‐I and mitochondrial antiviral signaling (MAVS) protein trigger a series of corresponding immune responses such as the production of type I interferon against viral infection. In this review, we are summarizing the role of the structural, nonstructural, and accessory proteins from SARS‐CoV‐2 on the RIG‐I‐MAVS pathway, and exploring the potential mechanism how SARS‐CoV‐2 could evade the host antiviral response. We then proposed that modulation of the RIG‐I‐MAVS signaling pathway might be a novel and effective therapeutic strategy to against COVID‐19 as well as the constantly mutating coronavirus.