Cell https://doi.org/10.1016/j.cell.2020.04.026 (2020)

The host response to the pandemic virus SARS-CoV-2 is still being defined. In Cell, tenOever and colleagues describe the SARS-CoV-2 host response and compare it to the responses to related coronaviruses MERS and SARS-CoV-1 and to more common respiratory viruses such as RSV and influenza A. Using cell lines, ex vivo human bronchial epithelium and a permissive ferret model of infection, the authors find that SARS-CoV-2 elicits a transcriptional response that is distinct from the other respiratory viruses examined. SARS-CoV-2 results in weak or absent antiviral type I and type III interferon (IFN) responses but strongly induces the proinflammatory cytokines IL (interleukin)-1β and IL-6, as well as the chemokines CCL2 and CXCL8. Some of the chemokines produced are potent monocyte/macrophage and neutrophil attractants, suggesting that these cells might play important roles in the pathology of COVID-19. Finally, broadly similar patterns of strong inflammatory cytokine and weak IFN expression are seen in human post-mortem lung tissue and serum from COVID-19-positive patients. These findings suggest that antagonizing select proinflammatory cytokines might be beneficial in treating COVID-19 symptoms.