A 193-amino acid fragment of the SARS coronavirus S protein efficiently binds angiotensin-converting enzyme 2.

Swee Kee Wong1 Wenhui Li Michael J Moore Hyeryun Choe Michael Farzan
Affiliations 1 institutions
  1. Partners AIDS Research Center, Brigham and Women's Hospital, Department of Medicine (Microbiology and Molecular Genetics), Harvard Medical School, Boston, Massachusetts 02115, USA.
Active Last checked 2026-09-29 03:30:37 Source: NCBI PubMed

Abstract

The coronavirus spike (S) protein mediates infection of receptor-expressing host cells and is a critical target for antiviral neutralizing antibodies. Angiotensin-converting enzyme 2 (ACE2) is a functional receptor for the coronavirus (severe acute respiratory syndrome (SARS)-CoV) that causes SARS. Here we demonstrate that a 193-amino acid fragment of the S protein (residues 318-510) bound ACE2 more efficiently than did the full S1 domain (residues 12-672). Smaller S protein fragments, expressing residues 327-510 or 318-490, did not detectably bind ACE2. A point mutation at aspartic acid 454 abolished association of the full S1 domain and of the 193-residue fragment with ACE2. The 193-residue fragment blocked S protein-mediated infection with an IC(50) of less than 10 nm, whereas the IC(50) of the S1 domain was approximately 50 nm. These data identify an independently folded receptor-binding domain of the SARS-CoV S protein.

Supporting text Virus Host Location
Alanine 2 Angiotensin-Converting Enzyme 2 178 Carboxypeptidases 6 Cell Line 162 Cysteine 2 Dose-Response Relationship, Drug 1 Electrophoresis, Polyacrylamide Gel 1 Flow Cytometry 4 Glutamic Acid 2 Humans 1455 Inhibitory Concentration 50 1 Membrane Glycoproteins 26 Mutation 211 Peptidyl-Dipeptidase A 58 Point Mutation 7 Protein Binding 194 Protein Structure, Tertiary 29 Severe acute respiratory syndrome-related coronavirus 79 Spike Glycoprotein, Coronavirus 276 Transfection 6 Viral Envelope Proteins 61 ACE2 protein, human 87 spike glycoprotein, SARS-CoV 16 spike protein, mouse hepatitis virus 7

Evidence records

1 total
Functional Mechanism
1 records · 1 evidence types
Evidence type
1 records
OVE11448
Key finding

A point mutation at Asp454 in the SARS-CoV spike S1 domain abolishes binding of the receptor-binding fragment to ACE2, defining a structural determinant for receptor interaction.

Virus
Host
Not specified
Location
Not specified
Supporting text

A point mutation at aspartic acid 454 abolished association of the full S1 domain and of the 193-residue fragment with ACE2. These data identify an independently folded receptor-binding domain of the SARS-CoV S protein.

Genes or proteins
Spike protein | S1 domain | 193-residue fragment (residues 318–510)
Receptors
ACE2
Mutations
Asp454 point mutation
Mechanism types
receptor binding | receptor usage | host entry