PLX208548

GSE147507: Transcriptional response of human lung epithelial cells to SARS-CoV-2 infection

• Organsim human
• Type RNASEQ
• Target gene
• Project COVID-19 transcriptomics

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 and ex vivo model systems. Our data demonstrate that each virus elicits both core antiviral components as well as unique transcriptional footprints. Compared to the response to influenza A virus (IAV) and respiratory syncytial virus (RSV), 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. SOURCE: Daniel Blanco MelotenOever Lab Icahn School of Medicine at Mount Sina