Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis
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- Lisa E. Gralinski
- Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA
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- Timothy P. Sheahan
- Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA
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- Thomas E. Morrison
- Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado, USA
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- Vineet D. Menachery
- Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA
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- Kara Jensen
- Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA
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- Sarah R. Leist
- Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA
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- Alan Whitmore
- Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, USA
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- Mark T. Heise
- Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, USA
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- Ralph S. Baric
- Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA
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- Kanta Subbarao
- editor
説明
<jats:p>The complement system is a critical part of host defense to many bacterial, viral, and fungal infections. It works alongside pattern recognition receptors to stimulate host defense systems in advance of activation of the adaptive immune response. In this study, we directly test the role of complement in SARS-CoV pathogenesis using a mouse model and show that respiratory disease is significantly reduced in the absence of complement even though viral load is unchanged. Complement-deficient mice have reduced neutrophilia in their lungs and reduced systemic inflammation, consistent with the observation that SARS-CoV pathogenesis is an immune-driven disease. These data suggest that inhibition of complement signaling might be an effective treatment option following coronavirus infection.</jats:p>
収録刊行物
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- mBio
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mBio 9 (5), 2018-11-07
American Society for Microbiology
