Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19
Author(s) -
Daniel Blanco-Melo,
Benjamin E. Nilsson-Payant,
WenChun Liu,
Skyler Uhl,
Daisy A. Hoagland,
Rasmus Møller,
Tristan X. Jordan,
Kohei Oishi,
Maryline Panis,
David Sachs,
Taia T. Wang,
Robert E. Schwartz,
Jean K. Lim,
Randy A. Albrecht,
Benjamin R. tenOever
Publication year - 2020
Publication title -
cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 26.304
H-Index - 776
eISSN - 1097-4172
pISSN - 0092-8674
DOI - 10.1016/j.cell.2020.04.026
Subject(s) - biology , chemokine , immunology , pandemic , virology , covid-19 , innate immune system , ex vivo , inflammatory response , transcriptome , cytokine , host response , in vivo , gene expression profiling , inflammation , gene expression , immune system , gene , infectious disease (medical specialty) , genetics , disease , medicine , pathology
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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