Shijie Qin1, Xinyi Xia2,3,4, Xuejia Shi1, Xinglai Ji5, Fei Ma1, Liming Chen1. 1. Department of Biochemistry, School of Life Sciences, Nanjing Normal University, Nanjing 210023, China. 2. COVID-19 Research Center, Institute of Laboratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing University and Southern Medical University, Nanjing 210002, China. 3. Department of Laboratory Medicine & Blood Transfusion, Wuhan Huoshenshan Hospital, Wuhan 430100, China. 4. Joint Expert Group for COVID-19, Wuhan Huoshenshan Hospital, Wuhan 430100, China. 5. Smart Health Big Data Analysis and Location Services Engineering Lab of Jiangsu Province, School of Geographic and Biologic Information, Nanjing University of Posts and Telecommunications, Nanjing 210023, China.
Abstract
SUMMARY: There are seven known coronaviruses that infect humans: four mild coronaviruses, including HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1, only cause mild respiratory diseases, and three severe coronaviruses, including SARS-CoV, MERS-CoV and SARS-CoV-2, can cause severe respiratory diseases even death of infected patients. Both infection and death caused by SARS-CoV-2 are still rapidly increasing worldwide. In this study, we demonstrate that viral coding proteins of SARS-CoV-2 have distinct features and are most, medium and least conserved with SARS-CoV, MERS-CoV and the rest four mild coronaviruses (HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1), respectively. Moreover, expression of host responsive genes (HRG), HRG-enriched biological processes and HRG-enriched KEGG pathways upon infection of SARS-CoV-2 shows slightly overlapping with SARS-CoV and MERS-CoV but distinctive to the four mild coronaviruses. Interestingly, enrichment of overactivation of neutrophil by HRGs is only and commonly found in infections of severe SARS-CoV-2, SARS-CoV and MERS-CoV but not in the other four mild coronaviruses, and the related gene networks show different patterns. Clinical data support that overactivation of neutrophil for severe patients can be one major factor for the similar clinical symptoms observed in SARS-CoV-2 infection compared to infections of the other two severe coronavirus (SARS-CoV and MERS-CoV). Taken together, our study provides a mechanistic insight into SARS-CoV-2 epidemic via revealing the conserved and distinct features of SARS-CoV-2, raising the critical role of dysregulation of neutrophil for SARS-CoV-2 infection. AVAILABILITY AND IMPLEMENTATION: All data sources and analysis methods related to this manuscript are available in the methods, supplementary materials and GEO database (https://www.ncbi.nlm.nih.gov/geo/). SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.
SUMMARY: There are seven known coronaviruses that infect humans: four mild coronaviruses, including HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1, only cause mild respiratory diseases, and three severe coronaviruses, including SARS-CoV, MERS-CoV and SARS-CoV-2, can cause severe respiratory diseases even death of infectedpatients. Both infection and death caused by SARS-CoV-2 are still rapidly increasing worldwide. In this study, we demonstrate that viral coding proteins of SARS-CoV-2 have distinct features and are most, medium and least conserved with SARS-CoV, MERS-CoV and the rest four mild coronaviruses (HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1), respectively. Moreover, expression of host responsive genes (HRG), HRG-enriched biological processes and HRG-enriched KEGG pathways upon infection of SARS-CoV-2 shows slightly overlapping with SARS-CoV and MERS-CoV but distinctive to the four mild coronaviruses. Interestingly, enrichment of overactivation of neutrophil by HRGs is only and commonly found in infections of severe SARS-CoV-2, SARS-CoV and MERS-CoV but not in the other four mild coronaviruses, and the related gene networks show different patterns. Clinical data support that overactivation of neutrophil for severe patients can be one major factor for the similar clinical symptoms observed in SARS-CoV-2 infection compared to infections of the other two severe coronavirus (SARS-CoV and MERS-CoV). Taken together, our study provides a mechanistic insight into SARS-CoV-2 epidemic via revealing the conserved and distinct features of SARS-CoV-2, raising the critical role of dysregulation of neutrophil for SARS-CoV-2 infection. AVAILABILITY AND IMPLEMENTATION: All data sources and analysis methods related to this manuscript are available in the methods, supplementary materials and GEO database (https://www.ncbi.nlm.nih.gov/geo/). SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.