Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis

Author:

Gralinski Lisa E.1,Sheahan Timothy P.1,Morrison Thomas E.2,Menachery Vineet D.13,Jensen Kara1,Leist Sarah R.1,Whitmore Alan4,Heise Mark T.4,Baric Ralph S.1

Affiliation:

1. Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA

2. Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado, USA

3. Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA

4. Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, USA

Abstract

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.

Funder

HHS | NIH | National Institute of Allergy and Infectious Diseases

Publisher

American Society for Microbiology

Subject

Virology,Microbiology

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