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@ARTICLE{Doldan:181787,
      author       = {P. Doldan$^*$ and J. Dai and C. Metz-Zumaran and J. T.
                      Patton and M. L. Stanifer and S. Boulant$^*$},
      title        = {{T}ype {III} and {N}ot {T}ype {I} {I}nterferons
                      {E}fficiently {P}revent the {S}pread of {R}otavirus in
                      {H}uman {I}ntestinal {E}pithelial {C}ells.},
      journal      = {Journal of virology},
      volume       = {96},
      number       = {17},
      issn         = {0022-538X},
      address      = {Baltimore, Md.},
      publisher    = {Soc.},
      reportid     = {DKFZ-2022-02210},
      pages        = {e00706-22},
      year         = {2022},
      note         = {#EA:F140#LA:F140#},
      abstract     = {Rotavirus infects intestinal epithelial cells and is the
                      leading cause of gastroenteritis in infants worldwide. Upon
                      viral infection, intestinal cells produce type I and type
                      III interferons (IFNs) to alert the tissue and promote an
                      antiviral state. These two types of IFN bind to different
                      receptors but induce similar pathways that stimulate the
                      activation of interferon-stimulated genes (ISGs) to combat
                      viral infection. In this work, we studied the spread of a
                      fluorescent wild-type (WT) SA11 rotavirus in human
                      colorectal cancer cells lacking specific interferon
                      receptors and compared it to that of an NSP1 mutant
                      rotavirus that cannot interfere with the host intrinsic
                      innate immune response. We could show that the WT rotavirus
                      efficiently blocks the production of type I IFNs but that
                      type III IFNs are still produced, whereas the NSP1 mutant
                      rotavirus allows the production of both. Interestingly,
                      while both exogenously added type I and type III IFNs could
                      efficiently protect cells against rotavirus infection,
                      endogenous type III IFNs were found to be key to limit
                      infection of human intestinal cells by rotavirus. By using a
                      fluorescent reporter cell line to highlight the cells
                      mounting an antiviral program, we could show that paracrine
                      signaling driven by type III IFNs efficiently controls the
                      spread of both WT and NSP1 mutant rotavirus. Our results
                      strongly suggest that NSP1 efficiently blocks the type I
                      IFN-mediated antiviral response; however, its restriction of
                      the type III IFN-mediated one is not sufficient to prevent
                      type III IFNs from partially inhibiting viral spread in
                      intestinal epithelial cells. Additionally, our findings
                      further highlight the importance of type III IFNs in
                      controlling rotavirus infection, which could be exploited as
                      antiviral therapeutic measures. IMPORTANCE Rotavirus is one
                      of the most common causes of gastroenteritis worldwide. In
                      developing countries, rotavirus infections lead to more than
                      200,000 deaths in infants and children. The intestinal
                      epithelial cells lining the gastrointestinal tract combat
                      rotavirus infection by two key antiviral compounds known as
                      type I and III interferons. However, rotavirus has developed
                      countermeasures to block the antiviral actions of the
                      interferons. In this work, we evaluated the arms race
                      between rotavirus and type I and III interferons. We
                      determined that although rotavirus could block the induction
                      of type I interferons, it was unable to block type III
                      interferons. The ability of infected cells to produce and
                      release type III interferons leads to the protection of the
                      noninfected neighboring cells and the clearance of rotavirus
                      infection from the epithelium. This suggests that type III
                      interferons are key antiviral agents and could be used to
                      help control rotavirus infections in children.},
      keywords     = {Antiviral Agents: pharmacology / Child / Epithelial Cells /
                      Gastroenteritis: metabolism / Humans / Interferon Type I:
                      metabolism / Interferons: metabolism / Rotavirus: metabolism
                      / Rotavirus Infections: metabolism / autocrine signaling
                      (Other) / human intestinal epithelial cells (Other) /
                      interferons (Other) / lambda interferon (IFN) (Other) /
                      paracrine signaling (Other) / rotavirus (Other) / rotavirus
                      NSP1 (Other) / type III interferon (IFN) (Other) / Antiviral
                      Agents (NLM Chemicals) / Interferon Type I (NLM Chemicals) /
                      Interferons (NLM Chemicals)},
      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:36000839},
      pmc          = {pmc:PMC9472630},
      doi          = {10.1128/jvi.00706-22},
      url          = {https://inrepo02.dkfz.de/record/181787},
}