Imbalanced host response to SARS-CoV-2 drives development of
COVID-19
Daniel Blanco-Melo1,2,*
, Benjamin E. Nilsson-Payant1,2,*
, Wen-Chun Liu1,3,*
, Skyler Uhl1,2
, Daisy
DOI: 10.1016/j.cell.2020.04.026
SUMMARY
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 indepth analysis of the transcriptional response to SARS-CoV-2 as it compares to other
respiratory viruses. Cell and animal models of SARS-CoV-2 infections, 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 IL6. Taken together, we propose that reduced innate antiviral defenses coupled
with exuberant inflammatory cytokine production are the defining and driving feature
of COVID-19.
