Fibrinogen as a Molecular Bridge Linking SARS-CoV-2 Immune Evasion and Endothelial Access?

Abstract

SARS-CoV-2 exploits multiple cellular entry routes. Beyond ACE2-mediated entry, we propose that the spike protein binds fibrinogen not only to facilitate immune evasion but also to position the receptor-binding domain for integrin-mediated uptake. This molecular bridge may enhance viral RNA delivery to endothelial cells. Targeting the spike protein–fibrinogen interface could open new therapeutic avenues for acute and post-COVID vascular disease.