Semmelweis University, Department of Molecular Biology at the Institute of Biochemistry and Molecular Biology, Budapest, Hungary.
Earlham Institute, Norwich Research Park, Norwich, United Kingdom.
PLoS One. 2022 Apr 7;17(4):e0266337. doi: 10.1371/journal.pone.0266337. eCollection 2022.
The COVID-19 pandemic caused by SARS-CoV-2 has resulted in an urgent need for identifying potential therapeutic drugs. In the first half of 2020 tropic antimalarial drugs, such as chloroquine (CQ) or hydroxochloroquine (HCQ) were the focus of tremendous public attention. In the initial periods of the pandemic, many scientific results pointed out that CQ/HCQ could be very effective for patients with severe COVID. While CQ and HCQ have successfully been used against several diseases (such as malaria, autoimmune disease and rheumatic illnesses); long term use of these agents are associated with serious adverse effects (i.e. inducing acute kidney injury, among many others) due to their role in blocking autophagy-dependent self-degradation. Recent experimental and clinical trial data also confirmed that there is no sufficient evidence about the efficient usage of CQ/HCQ against COVID-19. By using systems biology techniques, here we show that the cellular effect of CQ/HCQ on autophagy during endoplasmic reticulum (ER) stress or following SARS-CoV-2 infection results in upregulation of ER stress. By presenting a simple mathematical model, we claim that although CQ/HCQ might be able to ameliorate virus infection, the permanent inhibition of autophagy by CQ/HCQ has serious negative effects on the cell. Since CQ/HCQ promotes apoptotic cell death, here we confirm that addition of CQ/HCQ cannot be really effective even in severe cases. Only a transient treatment seemed to be able to avoid apoptotic cell death, but this type of therapy could not limit virus replication in the infected host. The presented theoretical analysis clearly points out the utility and applicability of systems biology modelling to test the cellular effect of a drug targeting key major processes, such as autophagy and apoptosis. Applying these approaches could decrease the cost of pre-clinical studies and facilitate the selection of promising clinical trials in a timely fashion.
由 SARS-CoV-2 引起的 COVID-19 大流行导致迫切需要确定潜在的治疗药物。在 2020 年上半年,抗疟药,如氯喹(CQ)或羟氯喹(HCQ)成为了巨大的公众关注焦点。在大流行的初期,许多科学研究结果指出,CQ/HCQ 可能对 COVID 重症患者非常有效。虽然 CQ 和 HCQ 已成功用于治疗几种疾病(如疟疾、自身免疫性疾病和风湿性疾病);但由于它们在阻断自噬依赖性自我降解中的作用,长期使用这些药物会导致严重的不良反应(如引起急性肾损伤等)。最近的实验和临床试验数据也证实,CQ/HCQ 对 COVID-19 的有效作用尚无足够证据。我们使用系统生物学技术表明,CQ/HCQ 在细胞内质网(ER)应激或 SARS-CoV-2 感染后对自噬的细胞作用导致 ER 应激上调。通过提出一个简单的数学模型,我们声称,尽管 CQ/HCQ 可能能够改善病毒感染,但 CQ/HCQ 对自噬的永久抑制对细胞有严重的负面影响。由于 CQ/HCQ 促进细胞凋亡死亡,因此我们证实,即使在严重情况下,添加 CQ/HCQ 也不能真正有效。只有短暂的治疗似乎才能避免细胞凋亡,但这种类型的治疗不能限制感染宿主中的病毒复制。本研究提出的理论分析清楚地指出了系统生物学建模在测试针对自噬和细胞凋亡等关键主要过程的药物的细胞作用方面的实用性和适用性。应用这些方法可以降低临床前研究的成本,并及时促进有前途的临床试验的选择。