Comments of the reviewer to letter of Zahra Abpeikar, Roohollah Mohseni & Mohsen Safaei: ‘The multifunctional nano-immunoliposome design: hypothesis on a therapeutic approach for COVID-19’

A. Rettenmeier
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Abstract

1. SARS-CoV-2 uses, among other things, the membrane-integrated ACE2 to enter the cell. Thus, ACE2 is a functional receptor for the virus. 2. Controlling or reducing the activity of this receptor (and of vimentin, a coreceptor) helps to influence the viral infection. 3. There is evidence that hypertension treatment with ACE inhibitors and angiotensin II receptor blockers (ARBs) causes an increased expression of ACE2. This leads to the hypothesis that patients treated with ACE inhibitors or ARBs may have an increased risk of SARS-CoV-2 infections or, in the case of infection, a worse prognosis. 4. The treatment of Vero E6 cells infected with the earlier SARS-CoV with IFNc and IL4 resulted in the down-regulation of ACE2. 5. The ACE2 inhibitor on the liposomes is needed to target the infected cells equipped with ACE2 receptors. 6. IFNc and IL4 should be used to neutralize the harmful increase in expression of ACE2 on the target cells caused by the ACE2 inhibitor on the liposomes.
审稿人对Zahra Abpeikar, Roohollah Mohseni和Mohsen Safaei的来信的评论:“多功能纳米免疫脂质体设计:关于COVID-19治疗方法的假设”
1. 除其他外,SARS-CoV-2利用膜整合的ACE2进入细胞。因此,ACE2是病毒的功能性受体。2. 控制或降低这种受体(以及一种辅助受体——波形蛋白)的活性有助于影响病毒感染。3.有证据表明,使用ACE抑制剂和血管紧张素II受体阻滞剂(ARBs)治疗高血压可导致ACE2表达增加。这导致了一种假设,即接受ACE抑制剂或arb治疗的患者感染SARS-CoV-2的风险可能增加,或者在感染的情况下,预后更差。4. IFNc和il - 4处理早期SARS-CoV感染的Vero E6细胞可导致ACE2的下调。5. 需要脂质体上的ACE2抑制剂靶向具有ACE2受体的感染细胞。6. 应使用IFNc和IL4来中和脂质体上的ACE2抑制剂引起的靶细胞上ACE2表达的有害增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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