Blood-clotting protein may be SARS-CoV-2's hidden accomplice, helping it hide from antibodies and reach blood vessels
Fibrinogen, the abundant plasma protein best known for forming blood clots, may play a second and far less benign role during SARS-CoV-2 infection: acting as a molecular bridge that simultaneously hides the virus from neutralizing antibodies and delivers it to the cells lining blood vessels.
Fibrinogen, a blood-clotting protein, may play a dual role in SARS-CoV-2 infections, according to a new hypothesis. Researchers from the University of Texas at Arlington and D Y Patil International University suggest that fibrinogen could act as a molecular bridge, simultaneously hiding the virus from neutralizing antibodies and delivering it to blood vessel cells.
This phenomenon may explain two key COVID-19 features: immune evasion and vascular damage. The spike protein of SARS-CoV-2 carries positively charged residues that could interact with negatively charged fibrinogen at physiological pH. When fibrinogen binds the spike protein, it can mask antigenic sites, providing protection against antibodies.
Concurrently, the gamma chain of fibrinogen engages endothelial receptors, forming a tether between the virus and the blood vessel wall. Molecular docking studies support this model, showing increased integrin binding and reduced ACE2 binding when fibrinogen is present. This proposed mechanism requires further experimental validation, but it could have clinical implications for treating vascular diseases related to COVID-19 and designing safer RNA delivery nanocarriers.
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