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Doris Wilflingseder1, Wilfried Posch1

  • 1Institut für Hygiene und Medizinische Mikrobiologie, Medizinische Universität Innsbruck, Schöpfstraße 41/R311, A-6020 Innsbruck, Österreich.

Biospektrum : Zeitschrift Der Gesellschaft Fur Biologishe Chemie (GBCH) Und Der Vereinigung Fur Allgemeine Und Angewandte Mikrobiologie (VAAM)
|February 23, 2022
PubMed
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Severe SARS-CoV-2 infection causes excessive inflammation via a new mechanism, linked to increased mortality. Complement overactivation contributes to lung injury in various coronavirus infections.

Area of Science:

  • Virology
  • Immunology
  • Pathology

Context:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is characterized by excessive inflammation.
  • This inflammation is driven by a novel mechanism, contributing to severe disease.
  • Complement system hyperactivation is implicated in lung injury across MERS-CoV, SARS-CoV-1, and SARS-CoV-2 infections.

Purpose:

  • To investigate the initial interactions between SARS-CoV-2 patient isolates and human respiratory epithelial tissues.
  • To utilize advanced 3D human respiratory tract models and lung organoids for studying early viral-host interactions.

Summary:

  • A novel inflammatory mechanism contributes to severe SARS-CoV-2 pathogenesis and mortality.
  • The study highlights the role of complement hyperactivation in coronavirus-induced lung injury.

Related Experiment Videos

  • 3D human respiratory models and lung organoids are effective tools for examining early SARS-CoV-2 interactions with host tissues.

    • Impact:

    • Provides insights into the mechanisms driving severe COVID-19.
    • Identifies potential therapeutic targets related to the complement system.
    • Establishes the utility of 3D organoid models for studying respiratory viral infections.