Insights on cross-species transmission of SARS-CoV-2 from structural modeling.

João P G L M Rodrigues1 Susana Barrera-Vilarmau2 João M C Teixeira3 Marija Sorokina4 Elizabeth Seckel5 Panagiotis L Kastritis4 Michael Levitt1
Affiliations 5 institutions
  1. Department of Structural Biology, Stanford University School of Medicine, Stanford, California, United States of America.
  2. Institute of Advanced Chemistry of Catalonia (IQAC), CSIC, Barcelona, Spain.
  3. Program in Molecular Medicine, The Hospital for Sick Children, Toronto, Ontario, Canada.
  4. ZIK HALOMEM & Institute of Biochemistry and Biotechnology, Martin Luther University Halle-Wittenberg, Biozentrum, Halle (Saale), Germany.
  5. Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, California, United States of America.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the ongoing global pandemic that has infected more than 31 million people in more than 180 countries worldwide. Like other coronaviruses, SARS-CoV-2 is thought to have been transmitted to humans from wild animals. Given the scale and widespread geographical distribution of the current pandemic and confirmed cases of cross-species transmission, the question of the extent to which this transmission is possible emerges, as well as what molecular features distinguish susceptible from non-susceptible animal species. Here, we investigated the structural properties of several ACE2 orthologs bound to the SARS-CoV-2 spike protein. We found that species known not to be susceptible to SARS-CoV-2 infection have non-conservative mutations in several ACE2 amino acid residues that disrupt key polar and charged contacts with the viral spike protein. Our models also allow us to predict affinity-enhancing mutations that could be used to design ACE2 variants for therapeutic purposes. Finally, our study provides a blueprint for modeling viral-host protein interactions and highlights several important considerations when designing these computational studies and analyzing their results.

COVID-19 425 SARS-CoV-2 453 Angiotensin-Converting Enzyme 2 177 Animals 1948 Binding Sites 89 Computational Biology 15 Conserved Sequence 7 Genetic Predisposition to Disease 1 Host-Pathogen Interactions 55 Humans 1440 Molecular Dynamics Simulation 21 Mutation 209 Spike Glycoprotein, Coronavirus 274 Viral Zoonoses 65 spike protein, SARS-CoV-2 157

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