冠状病毒病(COVID-19)导致多器官功能衰竭的病因学和免疫病理学问题

IF 0.1 Q4 MEDICINE, GENERAL & INTERNAL
T. Ashcheulova, N. Herasymchuk, O. A. Kochubiei, U. Herasymchuk
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引用次数: 0

摘要

COVID-19 的流行已被视为国际关注的紧急事件。这项研究的目的是分析、归纳和系统整理目前已有的关于新型冠状病毒感染在人体内发病机制研究的文献资料,并确定 SARS-CoV-2 侵入细胞后发生的关键变化。这样,医生就可以主要根据人体内发生的致病过程、治疗中观察到的综合征和症状复合体来确定治疗目标。文章通过文献综述证明,病毒与体细胞之间的特殊相互作用是冠状病毒感染发病机制的触发机制。血管紧张素转换酶 2(ACE2)受体是 SARS-CoV-2 进入人体的主要途径,该受体不仅在 2 型肺泡上皮细胞中表达,而且在肾脏、心脏、血管和胃肠道细胞中也有表达,包括内皮细胞和周细胞。在大脑的不同结构和部位、结膜细胞、边缘细胞、角膜细胞和固有层细胞中也有 ACE2 受体的表达。在口腔粘膜、唾液腺、扁桃体和舌头的上皮细胞中也发现了 ACE2 受体的高表达。这些因素解释了多器官功能衰竭可能涉及不同的器官和系统。在多器官功能衰竭的发展过程中,有两个重要因素:第一,直接细胞滋养和病毒载量,这可能是每个患者的独特之处。其次是对感染细胞的免疫介导反应。在高免疫炎症条件下,即细胞因子风暴发生时,急性呼吸窘迫综合征会发展,并出现多器官衰竭。内皮损伤直接参与了这一过程的病理生理学,导致发生内皮功能障碍、微循环破坏以及血管周围炎症,从而加重内皮损伤,并可能导致血栓形成。利用有关 COVID-19 免疫发病机制的现代知识,有助于估计严重感染的风险和可能出现的并发症,从而及时实施有效的病因治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Etiological and immunopathogenetic aspects of multiorgan failure development in coronavirus disease (COVID-19)
The COVID-19 epidemic has already come to be seen as an emergency of international concern. This relates not only to the wide occurrence of the infection, but also to a fairly high mortality rate, currently more than 6.5 million deaths in the world. The aim of this study was to analyze, generalize and systematize the currently available literary data on the study of the novel coronavirus infection pathogenesis in the human body and to determine key changes that occur after the SARS-CoV-2 penetration into cells. In this way to target physicians primarily based on the pathogenetic processes that occur in the human body, syndromes and symptom complexes that are observed in treatments. Results. The article presents a literature review demonstrating that the specific interaction between the virus and somatic cells is the triggering mechanism for the pathogenesis of coronavirus infection. The main route for SARS-CoV-2 entry into the body is the angiotensin-converting enzyme 2 (ACE2) receptor, which is expressed not only in type 2 alveolar epithelial cells, but also in cells of the kidney, heart, blood vessels and gastrointestinal tract, including endotheliocytes and pericytes. Expression of the ACE2 receptor has also been shown in various structures and parts of the brain, cells of the conjunctiva, limbus, cornea and cells of the substantia propria. A high expression of the ACE2 receptor has been found in the epithelial cells of the oral mucosa, salivary glands, tonsils and tongue. These factors explain a possible involvement of different organs and systems in the development of multiorgan failure. Conclusions. In the development of multiorgan disfunction, two components are important: first, direct cell tropism and viral load, that may be unique in each patient. Secondly, it is the development of immune-mediated reactions to infected cells. Under conditions of hyperimmune inflammation, that is, the development of cytokine storm, acute respiratory distress syndrome progresses, and multiple organ failure develops. Endothelial damage is directly involved in the pathophysiology of this process, that results in the development of endothelial dysfunction, disruption of microcirculation, as well as perivascular inflammation, which aggravates damage to the endothelium and can lead to thrombus formation. The use of modern knowledge about the immunopathogenesis of COVID-19 would help to estimate the risk for severe infection and the possible development of complications, allowing for the timely implementation of effective pathogenetic therapy.
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来源期刊
Zaporozhye Medical Journal
Zaporozhye Medical Journal MEDICINE, GENERAL & INTERNAL-
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