Modulation of SARS-CoV-2 Spike protein function by ADAM family proteases (MoCoSpA)

  • Funded by Bundesministerium für Bildung und Forschung [German Federal Ministry of Education and Research] (BMBF)
  • Total publications:1 publications

Grant number: 01KI20207

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  • Disease

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  • Funder

    Bundesministerium für Bildung und Forschung [German Federal Ministry of Education and Research] (BMBF)
  • Principle Investigator

  • Research Location

    Germany, Europe
  • Lead Research Institution

    RWTH Aachen University
  • Research Category

    Pathogen: natural history, transmission and diagnostics

  • Research Subcategory

    Pathogen morphology, shedding & natural history

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The SARS-CoV-2 spike protein interacts with angiotensin converting enzyme 2 (ACE-2) on epithelial cells in the lung which is a crucial step in viral infection and development of COVID2019. We propose that the metalloproteinases ADAM10 and ADAM17 are critical modulators of SARS-CoV-2 spike protein interaction with its receptor ACE-2 on lung epithelial cells. We want to study the induced release and functions of shed ACE-2 which may act as a soluble competitor and reduce the interaction of the virus with its membrane-anchored ACE-2 receptor. Moreover we want to study whether the spike protein triggers an inflammatory response by provoking increased ADAM-mediated shedding of proinflammatory mediators. These questions will be addressed in parallel by exposure of cultured epithelial cell lines and primary cells exposure to SARS-CoV-2 spike protein as well as by analysis of COVID19 patient tissues. For the analysis we will use established procedures to study ADAM activity, binding of adapter molecules, release of shed ACE-2, quantification of shed inflammatory mediators and cleavage of adhesion molecules. The analysis of these ADAM17 dependent responses shall help to understand why SARS-CoV-2 infection can cause a severe inflammatory response leading to ARDS with high mortality.

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The collectrin-like part of the SARS-CoV-1 and -2 receptor ACE2 is shed by the metalloproteinases ADAM10 and ADAM17.