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[From SARS to COVID-19: pathogens, receptor, pathogenesis and principles of the treatment].

Identifieur interne : 000404 ( PubMed/Curation ); précédent : 000403; suivant : 000405

[From SARS to COVID-19: pathogens, receptor, pathogenesis and principles of the treatment].

Auteurs : X. Wang [République populaire de Chine] ; Y Q Ding [République populaire de Chine]

Source :

RBID : pubmed:32238232

Abstract

COVID-19 is an infectious disease caused by 2019-nCoV and characterizes as an atypical pneumonia. Since 2019-nCoV is a newly emerging virus, the pathogenesis of COVID-19 is not well known. Most patients had a self-limited course, and some became severe even death. In this review, the authors compared two coronavirus outbreaks during the past two decades: the SARS-CoV and 2019-nCoV. Among the biological nature of the pathogens, viral receptor distribution on the human cells, and the pathological findings in the targeted organs and clinical features of the patients with the diseases, found similarities and differences between the two diseases. Due to the shared receptor ACE2 and the pathological similarities of the SARS-CoV and 2019-nCoV diseases. They proposed a pathogenesis model for COVID-19. Like the SARS-CoV disease, COVID-19 is a systematic disease and targets the lungs, vasculatures, and the immune system. The basic pathogenesis involves two interlinked processes: a severe lung inflammation and immune deficiency, both of which are related to an inappropriate immune response and over-production of cytokines. Thus, treatment approaches should include antiviral and anti-proinflammatory cytokines, anti-infectious and life support therapies, especially in patients with severe diseases.

DOI: 10.3760/cma.j.cn112151-20200318-00220
PubMed: 32238232

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pubmed:32238232

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<AbstractText>COVID-19 is an infectious disease caused by 2019-nCoV and characterizes as an atypical pneumonia. Since 2019-nCoV is a newly emerging virus, the pathogenesis of COVID-19 is not well known. Most patients had a self-limited course, and some became severe even death. In this review, the authors compared two coronavirus outbreaks during the past two decades: the SARS-CoV and 2019-nCoV. Among the biological nature of the pathogens, viral receptor distribution on the human cells, and the pathological findings in the targeted organs and clinical features of the patients with the diseases, found similarities and differences between the two diseases. Due to the shared receptor ACE2 and the pathological similarities of the SARS-CoV and 2019-nCoV diseases. They proposed a pathogenesis model for COVID-19. Like the SARS-CoV disease, COVID-19 is a systematic disease and targets the lungs, vasculatures, and the immune system. The basic pathogenesis involves two interlinked processes: a severe lung inflammation and immune deficiency, both of which are related to an inappropriate immune response and over-production of cytokines. Thus, treatment approaches should include antiviral and anti-proinflammatory cytokines, anti-infectious and life support therapies, especially in patients with severe diseases.</AbstractText>
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<AbstractText>新型冠状病毒感染疾病(COVID-19)是一种由人类新型冠状病毒(2019-nCoV)引起的传染病,基本特征以肺部炎性病变为主。目前正在全球迅速蔓延。该文比较近二十年间发生的两次人类冠状病毒严重急性呼吸综合征(SARS)和COVID-19肺炎的病原特点、受体分布、临床表现和病理改变,试图揭示COVID-19的病理生理机制,为治疗患者和疫情管控提供新思路。分析表明,由于2019-nCoV和SARS冠状病变在人体细胞上有相同的受体(ACE2),因而它们可能有相同的靶器官,如肺、心血管系统和免疫系统。病理改变除了病毒直接损伤靶器官中的功能细胞外,还与病毒诱导靶细胞产生促炎因子造成局部严重炎性反应有关。同时,促炎因子还过度激活了免疫细胞尤其是单核-巨噬细胞和T细胞,产生大量细胞因子形成细胞因子风暴(cytokine storm)。过量的细胞因子不但加剧了靶器官的炎性反应,还引起T细胞凋亡和免疫功能失调,造成免疫缺陷而不能有效清除病毒并造成继发感染。因此,在重症患者的管理上,除了生命支持及抗感染治疗外,有效控制肺部炎性反应和系统性拮抗细胞因子风暴可能有助于纠正缺氧,避免多器官衰竭乃至死亡。.</AbstractText>
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