Recently, Teams of Pro. Peihui Wang and Pro. Chengjiang Gao made new progress in the escape of the SARS-CoV-2 from human antiviral immunity and published a research paper entitled “Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) membrane (M) protein inhibits type I and III interferon production by targeting RIG-I/MDA-5 signaling” in Signal Transduction and Targeted Therapy, a subordinate journal of Nature. Dr. Yi Zheng, Basic Medical Sciences, and Mengxuan Zhuang, Advanced Medical Research Institute are co-authors, Pro. Peihui Wang and Pro. Chengjiang Gao are co-corresponding authors. Shandong University is the first unit of the paper.

The SARS-CoV-2 is a single-stranded RNA virus that can spread across species and infect humans. The COVID-19 caused by SARS-CoV-2 infection has become a global pandemic, with more than 82.66 million people infected as of December 31, 2020, with a cumulative death toll of more than 1.8 million, seriously endangering human health and creating an unprecedented threat to public health security and economic development. A typical feature of COVID-19 is that type I and III interferon-induced antiviral immunity is significantly suppressed and inflammatory responses are overactivated. How SARS-CoV-2 inhibits the molecular mechanism of human antiviral immunity has yet to be studied in depth.

This study found that SARS-CoV-2 membrane protein (membrane protein, M) inhibits type I and III interferon responses through the target intro topic RIG-I/MDA5 mediated RNA virus identification path, which in turn achieves immune escape, which may eventually lead to increased virus replication and transmission capabilities. Institutionally, SARS-CoV-2 M proteins can interact with RIG-I, MAVS, and TBK1 to prevent the formation of RIG-I, MAVS, TRAF3, and TBK1 protein complexes, thereby inhibiting phosphorylation, nucleation, and transcription activation induced by Type I and III interferons. This study expounds on the important mechanism of SARS-CoV-2 to suppress human antiviral immunity, provides a theoretical basis for interferon therapy to treat COVID-19, and reveals some pathogenic mechanisms of COVID-19.

The research work was supported by Shandong University's COVID-19 Emergency Research Project and the National Natural Science Foundation.

The paper link: https://pubmed.ncbi.nlm.nih.gov/33372174/