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@ARTICLE{MetzZumaran:179074,
      author       = {C. Metz-Zumaran and C. Kee$^*$ and P. Doldan$^*$ and C. Guo
                      and M. L. Stanifer and S. Boulant$^*$},
      title        = {{I}ncreased {S}ensitivity of {SARS}-{C}o{V}-2 to {T}ype
                      {III} {I}nterferon in {H}uman {I}ntestinal {E}pithelial
                      {C}ells.},
      journal      = {Journal of virology},
      volume       = {96},
      number       = {7},
      issn         = {0022-538X},
      address      = {Baltimore, Md.},
      publisher    = {Soc.},
      reportid     = {DKFZ-2022-00450},
      pages        = {e0170521},
      year         = {2022},
      note         = {#EA:F140#LA:F140# / 2022 Apr 13;96(7):e0170521},
      abstract     = {The coronavirus SARS-CoV-2 caused the COVID-19 global
                      pandemic leading to 5.3 million deaths worldwide as of
                      December 2021. The human intestine was found to be a major
                      viral target which could have a strong impact on virus
                      spread and pathogenesis since it is one of the largest
                      organs. While type I interferons (IFNs) are key cytokines
                      acting against systemic virus spread, in the human intestine
                      type III IFNs play a major role by restricting virus
                      infection and dissemination without disturbing homeostasis.
                      Recent studies showed that both type I and III IFNs can
                      inhibit SARS-CoV-2 infection, but it is not clear whether
                      one IFN controls SARS-CoV-2 infection of the human intestine
                      better or with a faster kinetics. In this study, we could
                      show that type I and III IFNs both possess antiviral
                      activity against SARS-CoV-2 in human intestinal epithelial
                      cells (hIECs); however, type III IFN is more potent. Shorter
                      type III IFN pretreatment times and lower concentrations
                      were required to efficiently reduce virus load compared to
                      type I IFNs. Moreover, type III IFNs significantly inhibited
                      SARS-CoV-2 even 4 h postinfection and induced a long-lasting
                      antiviral effect in hIECs. Importantly, the sensitivity of
                      SARS-CoV-2 to type III IFNs was virus specific since type
                      III IFN did not control VSV infection as efficiently.
                      Together, these results suggest that type III IFNs have a
                      higher potential for IFN-based treatment of SARS-CoV-2
                      intestinal infection compared to type I IFNs. IMPORTANCE
                      SARS-CoV-2 infection is not restricted to the respiratory
                      tract and a large number of COVID-19 patients experience
                      gastrointestinal distress. Interferons are key molecules
                      produced by the cell to combat virus infection. Here, we
                      evaluated how two types of interferons (type I and III) can
                      combat SARS-CoV-2 infection of human gut cells. We found
                      that type III interferons were crucial to control SARS-CoV-2
                      infection when added both before and after infection.
                      Importantly, type III interferons were also able to produce
                      a long-lasting effect, as cells were protected from
                      SARS-CoV-2 infection up to 72 h posttreatment. This study
                      suggested an alternative treatment possibility for
                      SARS-CoV-2 infection.},
      keywords     = {SARS-CoV-2 (Other) / human intestinal epithelial cells
                      (Other) / interferon (Other) / interferon lambda (Other) /
                      intrinsic immune response (Other) / type III interferon
                      (Other)},
      cin          = {F140},
      ddc          = {610},
      cid          = {I:(DE-He78)F140-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35262371},
      doi          = {10.1128/jvi.01705-21},
      url          = {https://inrepo02.dkfz.de/record/179074},
}