{"title":"SARS-CoV-2颠覆肺巨噬细胞抗病毒干扰素α反应?","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":"{\"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}","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
摘要
干扰素(ifn)是主要的抗病毒免疫因子。目前,各种干扰素疗法被用于治疗人类免疫缺陷病毒(HIV)、乙型肝炎(HBV)和丙型肝炎(HCV)、癌症和自身免疫性疾病。最近,有人建议使用IFN-α治疗来减轻SARS-CoV-2病毒感染(COVID-19)患者的呼吸道症状。SARS-CoV-2通过与血管紧张素转换酶2 (ACE2)结合进入细胞,ACE2通过识别病毒的刺突S1蛋白,充当病毒受体。由于ACE2的表达是由IFN-α诱导的,因此SARS-CoV-2病毒可能通过破坏IFN功能来利用抗病毒应答,从而进一步促进其自身的传播和传染性。我们在这里讨论了SARS-CoV-2如何破坏同样表达ACE2的肺巨噬细胞的免疫反应,从而加剧COVID-19呼吸道症状的严重程度。SARS-CoV-2颠覆肺巨噬细胞抗病毒干扰素α反应?Malgorzata kloc1,2,3 *, Rafik M. ghobrial1,2, Jacek Z kubiak4,5 * 1休斯顿循道卫理研究所,美国德克萨斯州休斯顿77030 2休斯顿循道卫理医院外科部,美国德克萨斯州休斯顿3德克萨斯大学安德森癌症中心遗传学部,美国德克萨斯州休斯顿4再生医学和细胞生物学实验室,军事卫生和流行病学研究所(WIHE),波兰华沙5 rennes大学,UMR 6290, CNRS,雷恩遗传与发育研究所,细胞周期组,雷恩医学院,法国
SARS-CoV-2 Subversion of the Antiviral Interferon Alpha-Response of Lung Macrophages?
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