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.

doi:10.1101/2022.01.02.474028

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bioRxiv · 10.1101/2022.01.02.474028

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.

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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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Nader, D., Gressett, T. E., Hossen, M. L., Chapagain, P. P., Kerrigan, S. W., Bix, G.. 2022-01-03. A dual-receptor mechanism between integrins and ACE2 widens SARS-CoV-2 tissue tropism. https://doi.org/10.1101/2022.01.02.474028

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