The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis
Open accessAbstract
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.
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Cites
Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene
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Complement: a key system for immune surveillance and homeostasis
Ricklin, D., Hajishengallis, G., Yang, K., & Lambris, J. D. (2010) · Nature Immunology · doi:10.1038/ni.1923 · Cited by 3,654 · cited 1×
“ways (15), and results in proteolytic processing of various components of the complement system, including C3, C4, and C5.”
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A Major Outbreak of Severe Acute Respiratory Syndrome in Hong Kong
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Characterization of a Novel Coronavirus Associated with Severe Acute Respiratory Syndrome
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Isolation and characterization of a bat SARS-like coronavirus that uses the ACE2 receptor
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Complement System Part I – Molecular Mechanisms of Activation and Regulation
Merle, N. S., Church, S. E., Fremeaux-Bacchi, V., & Roumenina, L. T. (2015) · Frontiers in Immunology · doi:10.3389/fimmu.2015.00262 · Cited by 1,620
Broad-spectrum antiviral GS-5734 inhibits both epidemic and zoonotic coronaviruses
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Interplay between inflammation and thrombosis in cardiovascular pathology
Stark, K., & Massberg, S. (2021) · Nature Reviews Cardiology · doi:10.1038/s41569-021-00552-1 · Cited by 1,033
Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19
Bonaventura, A., Vecchié, A., Dagna, L., Martinod, K., Dixon, D. L., Van Tassell, B. W., Dentali, F., Montecucco, F., Massberg, S., Levi, M., et al. (2021) · Nature Reviews Immunology · doi:10.1038/s41577-021-00536-9 · Cited by 987
A Mouse-Adapted SARS-CoV-2 Induces Acute Lung Injury and Mortality in Standard Laboratory Mice
Leist, S. R., Dinnon, K. H., Schäfer, A., Tse, L. V., Okuda, K., Hou, Y. J., West, A., Edwards, C. E., Sanders, W., Fritch, E. J., et al. (2020) · Cell · doi:10.1016/j.cell.2020.09.050 · Cited by 613
Self-citationAntibody-dependent enhancement and SARS-CoV-2 vaccines and therapies
Lee, W. S., Wheatley, A. K., Kent, S. J., & DeKosky, B. J. (2020) · Nature Microbiology · doi:10.1038/s41564-020-00789-5 · Cited by 676
Metadata
- Authors
- Gralinski, L. E., Sheahan, T. P., Morrison, T. E., Menachery, V. D., Jensen, K., Leist, S. R., Whitmore, A., Heise, M. T., & Baric, R. S.
- Venue
- mBio
- Publisher
- American Society for Microbiology
- Published
- 2018-11-07
- Volume
- 9
- Issue
- 5
- ISSN
- 2150-7511 (ISSN-L)
- 2161-2129
- OpenAlex
- W2898080189
- Cited by
- 655
- References
- 63
- FWCI
- 83.17
- Type
- journal article
- Language
- en
- Open access
- gold
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- Gralinski, L. E., Sheahan, T. P., Morrison, T. E., Menachery, V. D., Jensen, K., Leist, S. R., Whitmore, A., Heise, M. T., & Baric, R. S. (2018). Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis. mBio. https://doi.org/10.1128/mbio.01753-18
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.