Immune status and cytokine spectrum as predictors of the risk of severe disease and performance indicators of intensive therapy in patients with coronavirus infection covid-19

Q3 Medicine Health Risk Analysis Pub Date : 2022-12-01 DOI:10.21668/health.risk/2022.4.14
V.F. Sadykov, R. Poltavtseva, A. Chaplygina, N. Bobkova
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Abstract

The pandemic caused by a new strain of the SARS-CoV-2 coronavirus has swept the whole world but effective methods for treating this severe pathology have not yet been created. It has now been established that a risk of a severe course of COVID-19 is not so much a patient's age itself, but so-called age-related diseases; the renin-angiotensin system (RAS) is directly or indirectly involved into their development. The SARS-CoV-19 virus interacts with one of the main regulatory elements of this system, ACE2, and disrupts the balance between the two RAS branches. This ultimately manifests itself in an increase in levels of angiotensin II, which, through binding to the angiotensin type 1 receptor (AT1R), causes a number of pathological conditions, including hypertension, atherosclerosis, and cardiovascular diseases, enhances cell proliferation, apoptosis, death of vascular endothelial cells, etc. This process has been described in many reviews by Russian and foreign authors. However, cells of innate and adaptive immunity are another less well-described but no less important target of angiotensin II. The consequences of this interaction are analyzed in detail in this review. With COVID-19, dendritic cells are activated, macrophage proliferation and neutrophil infiltration increase with further involvement of CD4-lymphocytes and other cellular elements of the adaptive immunity in this process. Hyperactivation of the immune system is accompanied with the release of a large amount of pro-inflammatory cytokines, which can lead to the occurrence of a cytokine storm. The picture is aggravated by the inhibitory effect produced by the virus itself on the synthesis of signaling interferons at initial stages in its internalization into the cell. A separate section in the review ad-dresses the problem how to predict a risk of a developing serious condition and search for its predictors by analyzing the state of the RAS and ratios of key cellular elements in the immune system. This is extremely important for making decisions concerning the amount of necessary medical care and strategies for subsequent treatment.
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免疫状态和细胞因子谱作为冠状病毒感染新冠肺炎患者重症风险的预测因素和强化治疗的绩效指标
由新型冠状病毒SARS-CoV-2引起的大流行席卷全球,但目前还没有找到治疗这种严重病理的有效方法。现在已经确定,COVID-19严重病程的风险与其说是患者的年龄本身,不如说是所谓的年龄相关疾病;肾素-血管紧张素系统(RAS)直接或间接参与了它们的发育。SARS-CoV-19病毒与该系统的一个主要调控元件ACE2相互作用,并破坏两个RAS分支之间的平衡。这最终表现为血管紧张素II水平的升高,血管紧张素II通过与血管紧张素1型受体(AT1R)结合,引起高血压、动脉粥样硬化、心血管疾病等多种病理状况,增强细胞增殖、细胞凋亡、血管内皮细胞死亡等。俄罗斯和外国作者在许多评论中描述了这一过程。然而,先天免疫和适应性免疫细胞是血管紧张素II的另一个不太好描述但同样重要的靶点。这篇综述详细分析了这种相互作用的后果。在COVID-19中,树突状细胞被激活,巨噬细胞增殖和中性粒细胞浸润增加,cd4 -淋巴细胞等适应性免疫细胞因子在此过程中进一步参与。免疫系统的过度激活伴随着大量促炎细胞因子的释放,这可能导致细胞因子风暴的发生。在病毒内化进入细胞的初始阶段,病毒自身对信号干扰素合成的抑制作用使情况更加恶化。这篇综述的一个单独章节讨论了如何通过分析RAS的状态和免疫系统中关键细胞元素的比例来预测发展成严重疾病的风险,并寻找其预测因素。这对于决定必要的医疗护理数量和后续治疗策略极为重要。
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来源期刊
Health Risk Analysis
Health Risk Analysis Medicine-Health Policy
CiteScore
1.30
自引率
0.00%
发文量
38
审稿时长
20 weeks
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