The ORF3a protein of SARS-CoV-2 induces apoptosis in cells
Yujie Ren, Ting Shu, Di Wu, Jingfang Mu, Chong Wang, Muhan Huang, Yang Han, Xue-Yi Zhang, Wei Zhou, Yang Qiu & Xi Zhou
Cellular & Molecular Immunology (2020)Cite this article
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has caused the ongoing pandemic of Coronavirus Disease 2019. SARS-CoV-2 belongs to the genus Betacoronavirus of the Coronaviridae family, which includes SARS-CoV and Middle East respiratory syndrome coronavirus.1,2 Coronavirus-encoded accessory proteins play critical roles in virus–host interactions and the modulation of host immune responses, thereby contributing to coronaviral pathogenicity via different strategies.3 However, the functions of SARS-CoV-2-encoded accessory proteins are not well understood. Apoptosis is a predominant type of programmed cell death, and has been recognized as an important host antiviral defense mechanism that controls viral infection and regulates the inflammatory response.4,5 Previous studies have reported that the SARS-CoV-encoded accessory protein ORF3a can induce apoptosis in cells,6,7 leading to the question of whether SARS-CoV-2 ORF3a also has pro-apoptotic activity. Here, we investigated the potential apoptosis-inducing activity of SARS-CoV-2 ORF3a in different cell lines and compared the pro-apoptotic activities of SARS-CoV-2 ORF3a with those of SARS-CoV ORF3a using the same system.