This research found that the COVID-19 spike protein binds to the cell surface receptor GRP78.

If we could inject a large amount of GRP78 into patients could it saturate the virus particles, and inhibit the virus lifecycle?

If the injection of GRP78 would induce a severe immune response, could you administer immunosuppression, and rely on the deactivated viruses being filtered out of the blood by the kidneys and liver?

I know that this is a blunt object way to think about it. I'm really interested in the virus at the moment for obvious reasons, and hoping to learn more. Cheers!

1 Answer 1


The current data suggests that SARS-CoV-2 can enter cells by at least 4 methods:

  • ACE2 receptor - Angiotensin-converting enzyme 2 which is involved in protecting the lung (and other organs) from damage

  • CD147 - is a transmembrane glycoprotein that belongs to the immunoglobulin superfamily, which is involved in tumor development, plasmodium invasion and virus infection.

  • GRP78 receptors

  • Furin targets - an enzyme that works as a protein activator

Typically, a virus uses the outreaching spike protein to hook on to the host cell, but normally this protein is inactive. The cleavage site structure’s role is to trick the human furin protein, so it will cut and activate the spike protein and cause a “direct fusion” of the viral and cellular membranes.

The result findings show that when compared to the initial SARs mode of entry, this binding method is more than a 1,000 times efficient.

So, it seems possible that a neutralising antibody or protein could be produced that looks like the receptors on cell surfaces so that the virus preferentially binds to the neutralising antibody, and is thus deactivated.

Such drugs are available or in the drug pipeline and are awaiting clinical trials.



Your Answer

By clicking “Post Your Answer”, you agree to our terms of service and acknowledge you have read our privacy policy.

Not the answer you're looking for? Browse other questions tagged or ask your own question.