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

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.
Cell; 181(5): 1036-1045.e9, 2020 05 28.
Artículo en Inglés | MEDLINE | ID: mdl-32416070
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.