Department of Pharmacognosy, School of Pharmacy, China Medical University, Shenyang, China.
Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Front Immunol. 2022 Feb 4;13:798538. doi: 10.3389/fimmu.2022.798538. eCollection 2022.
Existing evidence demonstrates that coronavirus disease 2019 (COVID-19) leads to psychiatric illness, despite its main clinical manifestations affecting the respiratory system. People with mental disorders are more susceptible to COVID-19 than individuals without coexisting mental health disorders, with significantly higher rates of severe illness and mortality in this population. The incidence of new psychiatric diagnoses after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is also remarkably high. SARS-CoV-2 has been reported to use angiotensin-converting enzyme-2 (ACE2) as a receptor for infecting susceptible cells and is expressed in various tissues, including brain tissue. Thus, there is an urgent need to investigate the mechanism linking psychiatric disorders to COVID-19. Using a data set of peripheral blood cells from patients with COVID-19, we compared this to data sets of whole blood collected from patients with psychiatric disorders and used bioinformatics and systems biology approaches to identify genetic links. We found a large number of overlapping immune-related genes between patients infected with SARS-CoV-2 and differentially expressed genes of bipolar disorder (BD), schizophrenia (SZ), and late-onset major depressive disorder (LOD). Many pathways closely related to inflammatory responses, such as MAPK, PPAR, and TGF-β signaling pathways, were observed by enrichment analysis of common differentially expressed genes (DEGs). We also performed a comprehensive analysis of protein-protein interaction network and gene regulation networks. Chemical-protein interaction networks and drug prediction were used to screen potential pharmacologic therapies. We hope that by elucidating the relationship between the pathogenetic processes and genetic mechanisms of infection with SARS-CoV-2 with psychiatric disorders, it will lead to innovative strategies for future research and treatment of psychiatric disorders linked to COVID-19.
现有证据表明,2019 年冠状病毒病(COVID-19)可导致精神疾病,尽管其主要临床表现影响呼吸系统。与没有并存精神健康障碍的个体相比,患有精神障碍的人更容易感染 COVID-19,且该人群的重症和死亡率显著更高。感染严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)后新发精神疾病诊断的发生率也非常高。有报道称,SARS-CoV-2 利用血管紧张素转换酶-2(ACE2)作为感染易感细胞的受体,并且在包括脑组织在内的各种组织中表达。因此,迫切需要研究将精神障碍与 COVID-19 联系起来的机制。我们使用了一组 COVID-19 患者的外周血细胞数据集,并将其与从患有精神障碍的患者采集的全血数据集进行了比较,同时还使用了生物信息学和系统生物学方法来识别遗传联系。我们发现,感染 SARS-CoV-2 的患者与双相情感障碍(BD)、精神分裂症(SZ)和迟发性重度抑郁症(LOD)的差异表达基因之间存在大量重叠的免疫相关基因。通过对共同差异表达基因(DEG)进行富集分析,观察到许多与炎症反应密切相关的途径,如 MAPK、PPAR 和 TGF-β 信号通路。我们还对蛋白质-蛋白质相互作用网络和基因调控网络进行了全面分析。利用化学-蛋白质相互作用网络和药物预测来筛选潜在的药物治疗方法。我们希望通过阐明 SARS-CoV-2 感染与精神障碍的发病过程和遗传机制之间的关系,为未来与 COVID-19 相关的精神障碍的研究和治疗带来创新策略。