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Multiomics approach reveals the ubiquitination-specific processes hijacked by SARS-CoV-2.
Xu, Gang; Wu, Yezi; Xiao, Tongyang; Qi, Furong; Fan, Lujie; Zhang, Shengyuan; Zhou, Jian; He, Yanhua; Gao, Xiang; Zeng, Hongxiang; Li, Yunfei; Zhang, Zheng.
  • Xu G; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • Wu Y; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • Xiao T; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • Qi F; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • Fan L; Guangzhou Laboratory, Guangzhou Medical University, Guangzhou, China.
  • Zhang S; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • Zhou J; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • He Y; Department of Microbiology, Second Military Medical University, Shanghai Key Laboratory of Medical Biodefense, 200433, Shanghai, China.
  • Gao X; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • Zeng H; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • Li Y; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China.
  • Zhang Z; Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, 518112, Shenzhen, Guangdong Province, China. zhangzheng1975@aliyun.com.
Signal Transduct Target Ther ; 7(1): 312, 2022 09 07.
Article in English | MEDLINE | ID: covidwho-2008259
ABSTRACT
The Coronavirus Disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a global pandemic that seriously threatens health and socioeconomic development, but the existed antiviral drugs and vaccines still cannot yet halt the spread of the epidemic. Therefore, a comprehensive and profound understanding of the pathogenesis of SARS-CoV-2 is urgently needed to explore effective therapeutic targets. Here, we conducted a multiomics study of SARS-CoV-2-infected lung epithelial cells, including transcriptomic, proteomic, and ubiquitinomic. Multiomics analysis showed that SARS-CoV-2-infected lung epithelial cells activated strong innate immune response, including interferon and inflammatory responses. Ubiquitinomic further reveals the underlying mechanism of SARS-CoV-2 disrupting the host innate immune response. In addition, SARS-CoV-2 proteins were found to be ubiquitinated during infection despite the fact that SARS-CoV-2 itself didn't code any E3 ligase, and that ubiquitination at three sites on the Spike protein could significantly enhance viral infection. Further screening of the E3 ubiquitin ligases and deubiquitinating enzymes (DUBs) library revealed four E3 ligases influencing SARS-CoV-2 infection, thus providing several new antiviral targets. This multiomics combined with high-throughput screening study reveals that SARS-CoV-2 not only modulates innate immunity, but also promotes viral infection, by hijacking ubiquitination-specific processes, highlighting potential antiviral and anti-inflammation targets.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: SARS-CoV-2 / COVID-19 Topics: Vaccines Limits: Humans Language: English Journal: Signal Transduct Target Ther Year: 2022 Document Type: Article Affiliation country: S41392-022-01156-y

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Full text: Available Collection: International databases Database: MEDLINE Main subject: SARS-CoV-2 / COVID-19 Topics: Vaccines Limits: Humans Language: English Journal: Signal Transduct Target Ther Year: 2022 Document Type: Article Affiliation country: S41392-022-01156-y