Zhao Tie, Wang Chunhui, Duan Biyan, Yang Peipei, Wu Jianguo, Zhang Qiwei
Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, Guangzhou, China.
Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Hengyang Medical College, Institute of Pathogenic Biology, University of South China, Hengyang, China.
Front Microbiol. 2022 May 12;13:863802. doi: 10.3389/fmicb.2022.863802. eCollection 2022.
Coronavirus disease 2019 (COVID-19) is a global pandemic. Previous studies have reported dyslipidemia in patients with COVID-19. Herein, we conducted a retrospective study and a bioinformatics analysis to evaluate the essential data of the lipid profile as well as the possible mechanism in patients with COVID-19.
First of all, the retrospective study included three cohorts: patients with COVID-19, a healthy population, and patients with chronic obstructive pulmonary disease (COPD). For each subject, serum lipid profiles in the biochemical data were compared, including triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C). Furthermore, bioinformatics analyses were performed for exploring the biological or immunological mechanisms.
In line with the biochemical data of the three cohorts, the statistical result displayed that patients with COVID-19 were more likely to have lower levels of TC and HDL-C as compared with healthy individuals. The differential proteins associated with COVID-19 are involved in the lipid pathway and can target and regulate cytokines and immune cells. Additionally, a heatmap revealed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections were possibly involved in lipid metabolic reprogramming. The viral proteins, such as spike (S) and non-structural protein 2 (Nsp2) of SARS-CoV-2, may be involved in metabolic reprogramming.
The metabolic reprogramming after SARS-CoV-2 infections is probably associated with the immune and clinical phenotype of patients. Hence, metabolic reprogramming may be targeted for developing antivirals against COVID-19.
2019冠状病毒病(COVID-19)是一场全球大流行。先前的研究报道了COVID-19患者存在血脂异常。在此,我们进行了一项回顾性研究和生物信息学分析,以评估COVID-19患者血脂谱的基本数据以及可能的机制。
首先,回顾性研究包括三个队列:COVID-19患者、健康人群和慢性阻塞性肺疾病(COPD)患者。对每个受试者,比较生化数据中的血清血脂谱,包括甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C)。此外,进行生物信息学分析以探索生物学或免疫学机制。
与三个队列的生化数据一致,统计结果显示,与健康个体相比,COVID-19患者更有可能出现TC和HDL-C水平较低的情况。与COVID-19相关的差异蛋白参与脂质途径,并可靶向和调节细胞因子及免疫细胞。此外,热图显示严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染可能参与脂质代谢重编程。SARS-CoV-2的病毒蛋白,如刺突(S)蛋白和非结构蛋白2(Nsp2),可能参与代谢重编程。
SARS-CoV-2感染后的代谢重编程可能与患者的免疫和临床表型相关。因此,代谢重编程可能成为开发抗COVID-19抗病毒药物的靶点。