Author: Blanco-Melo, Daniel; Nilsson-Payant, Benjamin E.; Liu, Wen-Chun; Uhl, Skyler; Hoagland, Daisy; Møller, Rasmus; Jordan, Tristan X.; Oishi, Kohei; Panis, Maryline; Sachs, David; Wang, Taia T.; Schwartz, Robert E.; Lim, Jean K.; Albrecht, Randy A.; tenOever, Benjamin R.
Title: Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19 Cord-id: pcekcvwr Document date: 2020_5_15
ID: pcekcvwr
Snippet: 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
Document: 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. We propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19.
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