{"title":"SARS-CoV-2 Subversion of the Antiviral Interferon Alpha-Response of Lung Macrophages?","authors":"M. Kloc, R. Ghobrial, J. Kubiak","doi":"10.29245/2578-3009/2020/2.1189","DOIUrl":null,"url":null,"abstract":"The interferons (IFNs) are the main antiviral immune factors. Currently, various IFNs therapies are used for the treatment of human immunodeficiency virus (HIV), hepatitis B (HBV), and hepatitis C (HCV), cancer, and autoimmune diseases. Recently, it has been suggested that IFN-α therapy should be used to lessen the respiratory symptoms in the SARS-CoV-2 virusinfected (COVID-19) patients. The SARS-CoV-2 enters the cells by binding to the Angiotensinconverting enzyme 2 (ACE2), which by recognizing the spike S1 protein of the virus, acts as a virus receptor. Because the expression of ACE2 is induced by IFN-α, the SARS-CoV-2 virus may exploit the anti-viral response by subverting the IFN functions to further its own propagation and infectability. We discuss here how the SARS-CoV-2 may also subvert the immune response of the lung macrophages, which also express ACE2, to exacerbate the severity of the COVID-19 respiratory symptoms. SARS-CoV-2 Subversion of the Antiviral Interferon Alpha-Response of Lung Macrophages? Malgorzata Kloc1,2,3*, Rafik M. Ghobrial1,2, Jacek Z Kubiak4,5* 1The Houston Methodist Research Institute, Houston, Texas 77030, USA 2The Houston Methodist Hospital, Department of Surgery, Houston, Texas, USA 3The University of Texas, M.D. Anderson Cancer Center, Department of Genetics, Houston Texas, USA 4Laboratory of Regenerative Medicine and Cell Biology, Military Institute of Hygiene and Epidemiology (WIHE), Warsaw, Poland 5UnivRennes, UMR 6290, CNRS, Institute of Genetics and Development of Rennes, Cell Cycle Group, Faculty of Medicine, Rennes, France","PeriodicalId":73785,"journal":{"name":"Journal of immunological sciences","volume":"16 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2020-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of immunological sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.29245/2578-3009/2020/2.1189","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
The interferons (IFNs) are the main antiviral immune factors. Currently, various IFNs therapies are used for the treatment of human immunodeficiency virus (HIV), hepatitis B (HBV), and hepatitis C (HCV), cancer, and autoimmune diseases. Recently, it has been suggested that IFN-α therapy should be used to lessen the respiratory symptoms in the SARS-CoV-2 virusinfected (COVID-19) patients. The SARS-CoV-2 enters the cells by binding to the Angiotensinconverting enzyme 2 (ACE2), which by recognizing the spike S1 protein of the virus, acts as a virus receptor. Because the expression of ACE2 is induced by IFN-α, the SARS-CoV-2 virus may exploit the anti-viral response by subverting the IFN functions to further its own propagation and infectability. We discuss here how the SARS-CoV-2 may also subvert the immune response of the lung macrophages, which also express ACE2, to exacerbate the severity of the COVID-19 respiratory symptoms. SARS-CoV-2 Subversion of the Antiviral Interferon Alpha-Response of Lung Macrophages? Malgorzata Kloc1,2,3*, Rafik M. Ghobrial1,2, Jacek Z Kubiak4,5* 1The Houston Methodist Research Institute, Houston, Texas 77030, USA 2The Houston Methodist Hospital, Department of Surgery, Houston, Texas, USA 3The University of Texas, M.D. Anderson Cancer Center, Department of Genetics, Houston Texas, USA 4Laboratory of Regenerative Medicine and Cell Biology, Military Institute of Hygiene and Epidemiology (WIHE), Warsaw, Poland 5UnivRennes, UMR 6290, CNRS, Institute of Genetics and Development of Rennes, Cell Cycle Group, Faculty of Medicine, Rennes, France