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10.1016/j.cell.2020.04.026

http://scihub22266oqcxt.onion/10.1016/j.cell.2020.04.026
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32416070!7227586!32416070
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suck abstract from ncbi


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pmid32416070      Cell 2020 ; 181 (5): 1036-1045.e9
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  • Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19 #MMPMID32416070
  • Blanco-Melo D; Nilsson-Payant BE; Liu WC; Uhl S; Hoagland D; Moller R; Jordan TX; Oishi K; Panis M; Sachs D; Wang TT; Schwartz RE; Lim JK; Albrecht RA; tenOever BR
  • Cell 2020[May]; 181 (5): 1036-1045.e9 PMID32416070show ga
  • 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.
  • |Animals[MESH]
  • |Betacoronavirus/*physiology[MESH]
  • |COVID-19[MESH]
  • |Cells, Cultured[MESH]
  • |Chemokines/genetics/immunology[MESH]
  • |Coronavirus Infections/genetics/*immunology[MESH]
  • |Disease Models, Animal[MESH]
  • |Host-Pathogen Interactions[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Inflammation/virology[MESH]
  • |Interferons/genetics/immunology[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/genetics/*immunology[MESH]
  • |RNA Viruses/classification/*immunology[MESH]
  • |SARS-CoV-2[MESH]


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