Importance: Despite the availability of a vaccine against the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), humans will have to live with this virus and the after-effects of the coronavirus disease 2019 (COVID-19) infection for a long time. Cholesterol plays an important role in the infection and prognosis of SARS-CoV-2, and the study of its mechanism is of great significance not only for the treatment of COVID-19 but also for research on generic antiviral drugs. Observations: Cholesterol promotes the development of atherosclerosis by activating NLR family pyrin domain containing 3 (NLRP3), and the resulting inflammatory environment indirectly contributes to COVID-19 infection and subsequent deterioration. In in vitro studies, membrane cholesterol increased the number of viral entry sites on the host cell membrane and the number of angiotensin-converting enzyme 2 (ACE2) receptors in the membrane fusion site. Previous studies have shown that the fusion protein of the virus interacts with cholesterol, and the spike protein of SARS-CoV-2 also requires cholesterol to enter the host cells. Cholesterol in blood interacts with the spike protein to promote the entry of spike cells, wherein the scavenger receptor class B type 1 (SR-B1) plays an important role. Because of the cardiovascular protective effects of lipid-lowering therapy and the additional anti-inflammatory effects of lipid-lowering drugs, it is currently recommended to continue lipid-lowering therapy for patients with COVID-19, but the safety of extremely low LDL-C is questionable. Conclusions and Relevance: Cholesterol can indirectly increase the susceptibility of patients to SARS-CoV-2 and increase the risk of death from COVID-19, which are mediated by NLRP3 and atherosclerotic plaques, respectively. Cholesterol present in the host cell membrane, virus, and blood may also directly participate in the virus cell entry process, but the specific mechanism still needs further study. Patients with COVID-19 are recommended to continue lipid-lowering therapy.

中文翻译：

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胆固醇升高加重 COVID-19 的可能机制。

重要性：尽管有针对严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 的疫苗，但人类将不得不忍受这种病毒以及 2019 年冠状病毒病 (COVID-19) 感染的后遗症许久。胆固醇在SARS-CoV-2的感染和预后中起着重要作用，对其机制的研究不仅对COVID-19的治疗而且对仿制药的研究具有重要意义。观察：胆固醇通过激活含有 3 的 NLR 家族 pyrin 结构域（NLRP3）促进动脉粥样硬化的发展，由此产生的炎症环境间接导致 COVID-19 感染和随后的恶化。在体外研究中，膜胆固醇增加了宿主细胞膜上病毒进入位点的数量和膜融合位点中血管紧张素转换酶 2 (ACE2) 受体的数量。此前的研究表明，病毒的融合蛋白与胆固醇相互作用，SARS-CoV-2的刺突蛋白也需要胆固醇进入宿主细胞。血液中的胆固醇与刺突蛋白相互作用，促进刺突细胞进入，其中清道夫受体B型1（SR-B1）起着重要作用。由于降脂治疗的心血管保护作用和降脂药物的额外抗炎作用，目前推荐COVID-19患者继续降脂治疗，但极低LDL-C的安全性值得怀疑。结论和相关性：胆固醇可以间接增加患者对 SARS-CoV-2 的易感性并增加 COVID-19 的死亡风险，这分别由 NLRP3 和动脉粥样硬化斑块介导。存在于宿主细胞膜、病毒和血液中的胆固醇也可能直接参与病毒细胞进入过程，但具体机制仍有待进一步研究。建议 COVID-19 患者继续降脂治疗。