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Leveraging the antiviral type I interferon system as a first line of defense against SARS-CoV-2 pathogenicity

Authors
  • Hoagland, Daisy A.1
  • Møller, Rasmus1
  • Uhl, Skyler A.1
  • Oishi, Kohei1
  • Frere, Justin1
  • Golynker, Ilona1
  • Horiuchi, Shu1
  • Panis, Maryline1
  • Blanco-Melo, Daniel1
  • Sachs, David2
  • Arkun, Knarik3
  • Lim, Jean K.1
  • tenOever, Benjamin R.1
  • 1 Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
  • 2 Department of Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
  • 3 Department of Pathology and Laboratory Medicine, Tufts Medical Center, Boston, MA 02111, USA
Type
Published Article
Journal
Immunity
Publication Date
Jan 29, 2021
Volume
54
Issue
3
Pages
557–570
Identifiers
DOI: 10.1016/j.immuni.2021.01.017
PMID: 33577760
PMCID: PMC7846242
Source
PubMed Central
Keywords
License
Unknown

Abstract

The host response to SARS-CoV-2 results in significant inflammation. To understand this biology, Hoagland et al. utilize infected hamsters to elucidate transcriptional footprints across tissues longitudinally, showing an inflammatory response beyond the site of acute replication. Local administration of IFN-I reduces virus load and improves immune infiltrate.

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