Journal
CELL
Volume 181, Issue 5, Pages 1036-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2020.04.026
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Funding
- Marc Haas Foundation
- National Institutes of Health [5U19AI111825-07, 5R01AI139119-02, R01DK121072, R01AIAI145882, R01AI110575, R21AI149033]
- DARPA's PREPARE Program [HR0011-20-2-0040]
- Stanford University
- Searle Scholars Program
- CRIP (Center for Research on Influenza Pathogenesis), a NIAID [HHSN272201400008C]
- USPHS [T32-AI07647]
- NIH [R01 AI123155]
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Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2 compared with other respiratory viruses. Cell and animal models of SARS-CoV-2 infection, in addition to transcriptional and serum profiling of COVID-19 patients, consistently revealed a unique and inappropriate inflammatory response. This response is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high expression of IL-6. Wepropose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19.
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