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Jocher, G.* ; Grass, V.* ; Tschirner, S.K.* ; Riepler, L.* ; Breimann, S.* ; Kaya, T.* ; Oelsner, M. ; Hamad, M.S.* ; Hofmann, L.I.* ; Blobel, C.P.* ; Schmidt-Weber, C.B. ; Gokce, O.* ; Jakwerth, C.A. ; Trimpert, J.* ; Kimpel, J.* ; Pichlmair, A.* ; Lichtenthaler, S.F.*

ADAM10 and ADAM17 promote SARS-CoV-2 cell entry and spike protein-mediated lung cell fusion.

EMBO Rep. 23:e54305 (2022)

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The severe-acute-respiratory-syndrome-coronavirus-2 (SARS-CoV-2) is the causative agent of COVID-19, but host cell factors contributing to COVID-19 pathogenesis remain only partly understood. We identify the host metalloprotease ADAM17 as a facilitator of SARS-CoV-2 cell entry and the metalloprotease ADAM10 as a host factor required for lung cell syncytia formation, a hallmark of COVID-19 pathology. ADAM10 and ADAM17, which are broadly expressed in the human lung, cleave the SARS-CoV-2 spike protein (S) in vitro, indicating that ADAM10 and ADAM17 contribute to the priming of S, an essential step for viral entry and cell fusion. ADAM protease-targeted inhibitors severely impair lung cell infection by the SARS-CoV-2 variants of concern alpha, beta, delta, and omicron and also reduce SARS-CoV-2 infection of primary human lung cells in a TMPRSS2 protease-independent manner. Our study establishes ADAM10 and ADAM17 as host cell factors for viral entry and syncytia formation and defines both proteases as potential targets for antiviral drug development.

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