• Cell · May 2020

    Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19.

    • Daniel Blanco-Melo, Benjamin E Nilsson-Payant, Wen-Chun Liu, Skyler Uhl, Daisy Hoagland, Rasmus Møller, Tristan X Jordan, Kohei Oishi, Maryline Panis, David Sachs, Taia T Wang, Robert E Schwartz, Jean K Lim, Randy A Albrecht, and Benjamin R tenOever.
    • Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Virus Engineering Center for Therapeutics and Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
    • Cell. 2020 May 28; 181 (5): 1036-1045.e9.

    AbstractViral 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.Copyright © 2020 Elsevier Inc. All rights reserved.

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