Ubiquitination of SARS-CoV-2 ORF7a promotes antagonism of interferon response  

作　　者：Zengguo Cao Hongjie Xia Ricardo Rajsbaum Xianzhu Xia Hualei Wang Pei-Yong Shi 

机构地区：[1]Key Laboratory of Zoonosis Research,Ministry of Education,College of Veterinary Medicine,Jilin University,Changchun 130062,China [2]Department of Biochemistry and Molecular Biology,University of Texas Medical Branch,Galveston,TX 77555,USA [3]Department of Microbiology and Immunology,University of Texas Medical Branch,Galveston,TX 77555,USA [4]lnstitute for Human Infections and Immunity,University of Texas Medical Branch,Galveston,TX 77555,USA [5]Sealy Institute for Vaccine Sciences,University of Texas Medical Branch,Galveston,TX 77555,USA [6]Sealy Center for Structural Biology&Molecular Biophysics,University of Texas Medical Branch,Galveston,TX 77555,USA

出　　处：《Cellular & Molecular Immunology》2021年第3期746-748,共3页中国免疫学杂志（英文版）

摘　　要：Understanding interactions between the host and SARS-CoV-2 is essential for developing effective vaccines and therapeutics.Here,we report that SARS-CoV-2 usurps the host ubiquitin system to polyubiquitinate accessory protein ORF7a at Lys119.The 0RF7a polyubiquitination is primarily formed by K63-linked ubiquitin chains.

关 键 词：ORF7 INTERFERON primarily 

分 类 号：R563.1[医药卫生—呼吸系统]