Document Type
Article
Publication Date
3-18-2020
Abstract
Many human viral diseases are a consequence of a zoonotic event. Some of the diseases caused by these zoono- tic events have affected millions of people around the world, some of which have resulted in high rates of mor- bidity/mortality in humans. Changes in the viral proteins that function as ligands of the host receptor may pro- mote the spillover between species. The most recent of these zoonotic events that have caused an ongoing epi- demic of high magnitude is the Covid-19 epidemics caused by SARS-CoV-2. The aim of this study was to de- termine the mutation(s) in the sequence of the spike protein of the SARS-CoV-2 that might be favoring human to human transmission. An in silico approach was performed, and changes were detected in the S1 subunit of the receptor-binding domain of spike. The observed changes have significant effect on SARS-CoV-2 spike/ACE2 interaction and produce a reduction in the binding energy, compared to the one of the Bat-CoV to this receptor. The data presented in this study suggest a higher affinity of the SARS-Cov-2 spike protein to the human ACE2 receptor, compared to the one of Bat-CoV spike and ACE2. This could be the cause of the rapid viral spread of SARS-CoV-2 in humans.
Keywords
COVID-19 (disease), communicable diseases, coronavirus infections, spike, SARS-CoV-2, ACE2, coronavirus, outbreak
Publication Title
EXCLI Journal
Rights
© 2020 Ortega et al.This is an Open Access article distributed under the terms of the Creative Commons Attribution Licence (http://creativecommons.org/licenses/by/4.0/) You are free to copy, distribute and transmit the work, provided the original author and source are credited.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Recommended Citation
Ortega JT, Serrano ML, Pujol FH, Rangel HR. Role of changes in SARS-CoV-2 spike protein in the interaction with the human ACE2 receptor: An in silico analysis. EXCLI J. 2020 Mar 18;19:410-417. doi: 10.17179/excli2020-1167. PMID: 32210742; PMCID: PMC7081066.