bioRxivCell BiologyPreprint
A dual-receptor mechanism between integrins and ACE2 widens SARS-CoV-2 tissue tropism
D. Nader, T. E. Gressett, M. L. Hossen, P. P. Chapagain, S. W. Kerrigan, G. Bix
Abstract
In addition to the ACE2 receptor, SARS-CoV-2 binds to integrins to gain host cell entry and trigger pro-inflammatory integrin-mediated signalling cascades. Integrins, therefore, are likely candidates for a dual-receptor mechanism with ACE2 to explain the increased infectivity seen in SARS-CoV-2 models. As integrins are primarily expressed in vasculature and persistent vasculopathy is seen in COVID-19, examining the role of endothelial integrin involvement is crucial in uncovering the pathophysiology of SARS-CoV-2.
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