RT Journal Article
SR Electronic
T1 SARS-CoV-2 launches a unique transcriptional signature from in vitro, ex vivo, and in vivo systems
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.03.24.004655
DO 10.1101/2020.03.24.004655
A1 Daniel Blanco-Melo
A1 Benjamin E. Nilsson-Payant
A1 Wen-Chun Liu
A1 Rasmus Møller
A1 Maryline Panis
A1 David Sachs
A1 Randy A. Albrecht
A1 Benjamin R. tenOever
YR 2020
UL http://biorxiv.org/content/early/2020/03/24/2020.03.24.004655.abstract
AB One of the greatest threats to humanity is the emergence of a pandemic virus. Among those with the greatest potential for such an event include influenza viruses and coronaviruses. In the last century alone, we have observed four major influenza A virus pandemics as well as the emergence of three highly pathogenic coronaviruses including SARS-CoV-2, the causative agent of the ongoing COVID-19 pandemic. As no effective antiviral treatments or vaccines are presently available against SARS-CoV-2, it is important to understand the host response to this virus as this may guide the efforts in development towards novel therapeutics. Here, we offer the first in-depth characterization of the host transcriptional response to SARS-CoV-2 and other respiratory infections through in vitro, ex vivo, and in vivo model systems. Our data demonstrate the each virus elicits both core antiviral components as well as unique transcriptional footprints. Compared to the response to influenza A virus and respiratory syncytial virus, SARS-CoV-2 elicits a muted response that lacks robust induction of a subset of cytokines including the Type I and Type III interferons as well as a numerous chemokines. Taken together, these data suggest that the unique transcriptional signature of this virus may be responsible for the development of COVID-19.