The COVID-19 pandemic caused by SARS-CoV-2 is responsible for the global health emergency. Here, we explore the diverse mechanisms of SARS-CoV-induced inflammation. We presume that SARS-CoV-2 likely contributes analogous inflammatory responses. Possible therapeutic mechanisms for reducing SARS-CoV-2-mediated inflammatory responses comprise FcR inactivation. Currently, there is no specific remedy available against the SARS-CoV-2. Consequently, recognizing efficacious antiviral leads to combat the virus is crucially desired. The coronavirus (CoV) main protease (M^pro also called 3CL^pro), which plays an indispensable role in viral replication and transcription, is an interesting target for drug design. This review compiles the latest advances in biological and structural research, along with development of inhibitors targeting CoV M^pros. It is anticipated that inhibitors targeting CoV M^pros could be advanced into wide-spectrum antiviral drugs in case of COVID-19 and other CoV-related diseases. The crystal structural and docking results have shown that Ebselen, N3, TDZD-8 and α-ketoamide (13b) inhibitors can bind to the substrate-binding pocket of COVID-19 M^pro. α-ketoamide-based inhibitor 13b inhibits the replication of SARS-CoV-2 in human Calu3 lung cells. Quantitative real-time RT-PCR (qRT-PCR) showed that the treatment with Ebselen, TDZD-8 and N3 reduced the amounts of SARS-CoV-2, respectively, 20.3-, 10.19- and 8.4-fold compared to the treatment in the absence of inhibitor. Moreover, repurposing of already present drugs to treat COVID-19 serves as one of the competent and economic therapeutic strategies. Several anti-malarial, anti-HIV and anti-inflammatory drugs as mentioned in Table 2 were found effective for the COVID-19 treatment. Further, hydroxychloroquine (HCQ) was found more potent than chloroquine (CQ) in inhibiting SARS-CoV-2 in vitro. Furthermore, convalescent plasma from patients who have recuperated from viral infections can be employed as a therapy without the appearance of severe adverse events. Hence, it might be valuable to examine the safety and efficacy of convalescent plasma transfusion in SARS-CoV-2-infected patients.

由 SARS-CoV-2 引起的 COVID-19 大流行造成了全球卫生紧急情况。在这里，我们探讨了 SARS-CoV 诱导炎症的多种机制。我们推测 SARS-CoV-2 可能会引起类似的炎症反应。减少 SARS-CoV-2 介导的炎症反应的可能治疗机制包括 FcR 失活。目前，尚无针对 SARS-CoV-2 的特效疗法。因此，迫切需要识别有效的抗病毒药物来对抗病毒。冠状病毒（CoV）主要蛋白酶（M ^pro也称为 3CL ^pro）在病毒复制和转录中发挥着不可或缺的作用，是药物设计的一个有趣的靶点。这篇综述汇集了生物学和结构研究的最新进展，以及针对 CoV M ^pro的抑制剂的开发。预计针对 CoV M ^{pro 的}抑制剂可能会被开发成广谱抗病毒药物，以应对 COVID-19 和其他 CoV 相关疾病。晶体结构和对接结果表明，Ebselen、N3、TDZD-8 和 α-酮酰胺 ( 13b ) 抑制剂可以与 COVID-19 M ^pro的底物结合袋结合。基于 α-酮酰胺的抑制剂13b抑制人 Calu3 肺细胞中 SARS-CoV-2 的复制。实时定量 RT-PCR (qRT-PCR) 显示，与对照组相比，Ebselen、TDZD-8 和 N3 治疗后 SARS-CoV-2 的量分别减少了 20.3 倍、10.19 倍和 8.4 倍。缺乏抑制剂。此外，重新利用现有药物来治疗 COVID-19 是一种有效且经济的治疗策略。表2中提到的几种抗疟疾、抗HIV和抗炎药物被发现对治疗COVID-19有效。此外，羟氯喹 (HCQ) 在体外抑制 SARS-CoV-2 方面比氯喹 (CQ) 更有效。此外，从病毒感染中恢复过来的患者的恢复期血浆可以用作治疗，而不会出现严重的不良事件。因此，检查 SARS-CoV-2 感染患者恢复期血浆输注的安全性和有效性可能很有价值。