Abstract

Viruses have multiple mutation rates that are higher than any other member of the kingdom of life. This gives them the ability to evolve, even within the course of a single infection, and to evade multiple host defenses, thereby impacting pathogenesis. Additionally, there are also interplays between mutation and recombination and the high multiplicity of infection (MOI) that enhance viral adaptability and increase levels of recombination leading to complex and conflicting effects on genome selection, and the net results is difficult to predict. Recently, the outbreak of COVID-19 virus represents a pandemic threat that has been declared a public health emergency of international concern. Up to present, however, due to the high mutation rate of COVID-19 virus, there are no effective procedures to contain the spread of this virus across the globe. For such a purpose, there is then an urgent need to explore new approaches. As an opinion, the present approach emphasizes on (a) the use of a nonspecific way of blocking the entry of COVID-19 virus as well as its variants into the cells via a therapeutic biocompatible compound (ideally, “in a pill”) targeting its spike (S) glycoprotein; and (b) the construction of expression vectors via the glycosyl-phosphatidylinositol, GPI, anchor for studying intermolecular interactions between the spike S of COVID-19 virus as well as its variants and the angiotensin-converting enzyme 2 (ACE2) of its host receptor for checking the efficacy of any therapeutic biocompatible compound of the nonspecific way of blocking. Such antiviral drug would be safer than the ACE1 and ACE2 inhibitors/angiotensin receptor blockers, and recombinant human ACE2 as well as nucleoside analogs or protease inhibitors used for fighting the spread of the virus inside the cells, and it would also be used as a universal one for any eventual future pandemic related to viruses, especially the RNA viruses with high mutation rates.

摘要

病毒具有多种突变率，高于生命王国的任何其他成员。这使它们能够进化，即使是在一次感染过程中，也能避开多种宿主防御，从而影响发病机制。此外，突变和重组与高感染复数 (MOI) 之间也存在相互作用，从而增强病毒的适应性并提高重组水平，从而对基因组选择产生复杂和相互矛盾的影响，最终结果难以预测。最近，COVID-19 病毒的爆发代表了一种大流行威胁，已被宣布为国际关注的突发公共卫生事件。然而，到目前为止，由于 COVID-19 病毒的高突变率，没有有效的程序来遏制这种病毒在全球的传播。为此，迫切需要探索新的方法。作为一种观点，本方法强调 (a) 使用非特异性方法通过治疗性生物相容性化合物（理想情况下，“在药丸中”）靶向阻断 COVID-19 病毒及其变体进入细胞其刺突 (S) 糖蛋白；(b) 通过糖基磷脂酰肌醇 (GPI) 构建表达载体，该锚点用于研究 COVID-19 病毒的刺突 S 及其变体与其宿主受体的血管紧张素转换酶 2 (ACE2) 之间的分子间相互作用用于检查非特异性阻断方式的任何治疗性生物相容性化合物的功效。这种抗病毒药物比 ACE1 和 ACE2 抑制剂/血管紧张素受体阻滞剂更安全，