Abstract
SummaryCOVID-19 broke out in the end of December 2019 and is still spreading rapidly, which has been listed as an international concerning public health emergency. We found that the Spike protein of SARS-CoV-2 contains a furin cleavage site, which did not exist in any other betacoronavirus subtype B. Based on a series of analysis, we speculate that the presence of a redundant furin cut site in its Spike protein is responsible for SARS-CoV-2's stronger infectious nature than other coronaviruses, which leads to higher membrane fusion efficiency. Subsequently, a library of 4,000 compounds including approved drugs and natural products was screened against furin through structure-based virtual screening and then assayed for their inhibitory effects on furin activity. Among them, an anti-parasitic drug, diminazene, showed the highest inhibition effects on furin with an IC50 of 5.42 ± 0.11 μM, which might be used for the treatment of COVID-19.
Highlights
A novel coronavirus (SARS-CoV-2) infectious disease broke out in the end of December 2019 and is still spreading rapidly, which has been listed as an international concerning public health emergency
We found that the Spike protein of SARS-CoV-2 contains a furin cleavage site, which did not exist in any other betacoronavirus subtype B
Based on a series of analysis, we speculate that the presence of a redundant furin cut site in its Spike protein is responsible for SARS-CoV-2’s stronger infectious nature than other coronaviruses, which leads to higher membrane fusion efficiency
Summary
A novel coronavirus (SARS-CoV-2) infectious disease broke out in the end of December 2019 and is still spreading rapidly, which has been listed as an international concerning public health emergency. As of August 17, 2020, a total of 21,777,834 patients have been diagnosed and 776,544 have died worldwide. This disease is caused by a novel coronavirus, which was named ‘‘2019-nCoV’’ by the World Health Organization, and the disease caused by 2019-nCoV was named COVID-19. A trimeric glycoprotein of CoVs, determines the diversity of CoVs and host tropism and mediates CoVs’ binding to host cells surface-specific receptors and virus-cell membrane fusion (Lu et al, 2015). Current research found that SARS-CoV-2 belongs to the b-coronavirus genus and speculated that it may interact with angiotensin-converting enzyme 2 (ACE2) on the surface of human cells through Spike protein, thereby infecting human respiratory epithelial cell (Xu et al, 2020). Letko and Munster identified the receptor for SARS-CoV-2 entry into human cells to be ACE2 (Letko et al, 2020)
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