Pubmed文献速递|高血糖水平是2019冠状病毒疾病严重程度的主要危险因素
SARS-CoV-2在2019年底开始传播，导致2019冠状病毒疾病，这种疾病在几个月内就在人群中达到流行病的比例。不同人群之间疾病严重程度不同的原因，特别是为什么疾病对老龄人口和那些具有特定先决条件的人的影响更为严重，目前尚不清楚。
我们开发了机器学习模型，可以在 CORD-19数据库中公开访问240,000篇科学论文，并构建了知识图形，以综合提取的信息和浏览集体知识，试图寻找导致疾病严重程度的潜在共同潜在原因。文献反复指出血糖升高是2019冠状病毒疾病发展的关键促进因素。
事实上，当我们追溯 SARS-CoV-2感染的步骤时，我们发现有证据表明升高的葡萄糖与病毒生命周期的每一步、疾病的进展和症状的表现有关。具体来说，葡萄糖浓度的升高为病毒提供了理想的条件，以逃避和削弱肺部的第一层免疫防御系统，进入肺泡深处的细胞，与 ACE2受体结合并进入肺细胞，加速病毒在细胞内的复制，增加细胞死亡，并诱发肺部炎症反应，压倒已经减弱的先天免疫系统，引发系统性感染、炎症和细胞损伤、细胞因子风暴和血栓事件。
我们通过分析跨文献的数据，在肺部气道表面原子重建病毒，并对葡萄糖水平对感染过程的影响进行定量计算模拟，来验证这一假设的可行性。
我们的结论是，血糖水平的升高可以通过多种机制促进疾病的进展，并且可以解释在整个人群中所看到的疾病严重程度的差异。这项研究提出了诊断建议、新的研究领域和潜在的治疗方法，以及引起血糖水平升高的治疗策略和关键护理条件的注意事项。
SARS-CoV-2 started spreading towards the end of 2019 causing COVID-19, a disease that reached pandemic proportions among the human population within months. The reasons for the spectrum of differences in the severity of the disease across the population, and in particular why the disease affects more severely the aging population and those with specific preconditions are unclear. We developed machine learning models to mine 240,000 scientific papers openly accessible in the CORD-19 database, and constructed knowledge graphs to synthesize the extracted information and navigate the collective knowledge in an attempt to search for a potential common underlying reason for disease severity. The literature repeatedly pointed to elevated blood glucose as a key facilitator in the progression of COVID-19. Indeed, when we retraced the steps of the SARS-CoV-2 infection we found evidence linking elevated glucose to each step of the life-cycle of the virus, progression of the disease, and presentation of symptoms. Specifically, elevations of glucose provide ideal conditions for the virus to evade and weaken the first level of the immune defense system in the lungs, gain access to deep alveolar cells, bind to the ACE2 receptor and enter the pulmonary cells, accelerate replication of the virus within cells increasing cell death and inducing an pulmonary inflammatory response, which overwhelms an already weakened innate immune system to trigger an avalanche of systemic infections, inflammation and cell damage, a cytokine storm and thrombotic events. We tested the feasibility of the hypothesis by analyzing data across papers, reconstructing atomistically the virus at the surface of the pulmonary airways, and performing quantitative computational modeling of the effects of glucose levels on the infection process. We conclude that elevation in glucose levels can facilitate the progression of the disease through multiple mechanisms and can explain much of the variance in disease severity seen across the population. The study proposes diagnostic recommendations, new areas of research and potential treatments, and cautions on treatment strategies and critical care conditions that induce elevations in blood glucose levels.
doi: https://doi.org/10.1101/2021.04.29.21256294
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