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A Review: Does Complement or the Contact System Have a Role in Protection or Pathogenesis of COVID-19?

机译：审查：补充或联系系统是否具有Covid-19的保护或发病机制中的作用？

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IntroductionCOVID-19 presentation may include a profound increase in cytokines and associated pneumonia, rapidly progressing to acute respiratory distress syndrome (ARDS). This so-called cytokine storm often leads to refractory edema, respiratory arrest, and death. At present, anti-IL-6, antiviral therapy, convalescent plasma, hydroxychloroquine, and azithromycin among others are being investigated as potential treatments for COVID-19. As the disease etiology and precise therapeutic interventions are still not definitively defined, we wanted to review the roles that complement and the contact system may have in either the treatment or pathogenesis of the disease.MethodsWe searched the recent literature (PubMed) on complement and coronavirus; contact system and coronavirus; bradykinin and coronavirus; and angiotensin receptor and coronavirus. The manuscript complies with ethics guidelines and was deemed exempt from institutional review board approval according to Human Subjects Protection Office guidelines.ResultsMouse models are available for the study of coronavirus and complement. Although complement is effective in protecting against many viruses, it does not seem to be protective against coronavirus. C3 knockout mice infected with SARS-CoV had less lung disease than wild-type mice, suggesting that complement may play a role in coronavirus pathogenesis. Some evidence suggests that the observed pulmonary edema may be bradykinin-induced and could be the reason that corticosteroids, antihistamines, and other traditional interventions for edema are not effective. Angiotensin-converting enzyme 2 (ACE2) is a co-receptor for SARS-CoV-2, and studies thus far have not concluded a benefit or risk associated with the use of either ACE-inhibitors or angiotensin receptor antagonists.SummaryActivation of complement and the contact system, through generation of bradykinin, may play a role in the SARS-CoV-2-induced pulmonary edema, and our search suggests that further work is necessary to confirm our suspicions.
机译：介绍Covid-19介绍可能包括细胞因子和相关肺炎的深刻增加，迅速进展到急性呼吸窘迫综合征（ARDS）。这种所谓的细胞因子风暴通常导致难治性水肿，呼吸逮捕和死亡。目前，抗IL-6，抗病患者治疗，颠膜等离子体，羟基氯喹和阿奇霉素正在被研究作为Covid-19的潜在治疗方法。由于疾病病因和精确的治疗干预措施仍然没有明确定义，我们想审查补充和接触系统可能在疾病的治疗或发病机制中的作用。乙其对最近的文献（Pubmed）进行补充和冠状病毒;联系系统和冠状病毒; Bradykinin和冠状病毒;和血管紧张素受体和冠状病毒。稿件符合道德准则，并被视为豁免机构审查委员会批准，根据人类受试者保护办公室指南。对冠状病毒和补充的研究提供了研究。虽然补充是有效保护许多病毒，但它似乎对冠状病毒似乎没有保护。 C3被SARS-COV感染的敲除小鼠比野生型小鼠的肺部疾病较少，表明补体可能在冠状病毒发病机制中发挥作用。有些证据表明，观察到的肺水肿可能是Bradykinin-诱导的并且可能是皮质类固醇，抗组胺药和其他对水肿的传统干预措施的原因无效。血管紧张素转换酶2（ACE2）是SARS-COV-2的共同受体，因此研究的研究没有结论与使用ACE抑制剂或血管紧张素受体拮抗剂相关的益处或风险。umpressactivation补充和联系系统通过生成Bradykinin，可能在SARS-COV-2诱导的肺水肿中发挥作用，我们的搜索表明需要进一步的工作来确认我们的怀疑。

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