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A dual-receptor mechanism between integrins and ACE2 widens SARS-CoV-2 tissue tropism

Nader, D.; Gressett, T. E.; Hossen, M. L.; Chapagain, P. P.; Kerrigan, S. W.; Bix, G.

2022-01-03 cell biology
10.1101/2022.01.02.474028 bioRxiv
Show 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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