No evidence for basigin/CD147 as a direct SARS-CoV-2 spike binding receptor

Area of Science:

• Virology
• Molecular Biology
• Immunology

Background:

• The SARS-CoV-2 spike protein facilitates viral entry by binding to host cell receptors, primarily ACE2.
• Basigin/CD147 was recently proposed as an alternative SARS-CoV-2 entry receptor, prompting further investigation and clinical trials.

Purpose of the Study:

• To investigate the proposed role of basigin/CD147 as a SARS-CoV-2 entry receptor.
• To determine if the SARS-CoV-2 spike protein directly interacts with basigin/CD147.
• To assess the impact of basigin/CD147 on SARS-CoV-2 infection susceptibility.

Main Methods:

• Utilized recombinant SARS-CoV-2 spike proteins to test for binding to basigin expressed on human cells.
• Employed specialized assays to detect weak or strong interactions between spike protein and basigin isoforms.
• Used CRISPR/Cas9 gene editing to remove basigin from human lung epithelial cells.

Main Results:

• No direct interaction was observed between recombinant SARS-CoV-2 spike proteins and basigin/CD147.
• Specialized assays confirmed the absence of significant binding between spike protein and common basigin isoforms.
• Removal of basigin from lung epithelial cells did not alter their susceptibility to SARS-CoV-2 infection.

Conclusions:

• The findings do not support basigin/CD147 as a functional receptor for SARS-CoV-2 spike protein-mediated entry.
• This research clarifies the translational relevance of basigin/CD147 as a therapeutic target for COVID-19.
• The results aid in informed decision-making for developing effective SARS-CoV-2 antiviral strategies.