Imbalanced host response to SARS-CoV-2 drives development of COVID-19

Daniel Blanco-Melo, Benjamin E. Nilsson-Payant, Wen-Chun Liu, Skyler Uhl, Daisy Hoagland, Rasmus Møller, Tristan X. Jordan, Kohei Oishi, Maryline Panis, David Sachs, Taia T. Wang, Robert E. Schwartz, Jean K. Lim, Randy A. Albrecht, BenjaminR. tenOever
Source: Cell
Publication Date: (2020)
Issue: 182: 1-20
Research Area:
Gene Expression
Basic Research
Respiratory Research
Drug Discovery
Cells used in publication:
Epithelial, bronchial (NHBE), human
Species: human
Tissue Origin: lung

Undifferentiated normal human bronchial epithelial (NHBE) cells (Lonza, CC-2540 Lot# 580580) were isolated from a 79-year-old Caucasian female and were maintained in bronchial epithelial growth media (Lonza, CC-3171) supplemented with BEGM SingleQuots as per the manufacturer’s instructions (Lonza, CC-4175) at 37°C and 5% CO2.


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 IL-6. Taken together, we propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving feature of COVID-19.