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@ARTICLE{Adam:283165,
      author       = {L. Adam and M. Stanifer and F. Springer and J. Mathony and
                      M. Brune and C. Di Ponzio and R. Eils and S. Boulant$^*$ and
                      D. Niopek and S. Kallenberger$^*$},
      title        = {{T}ranscriptomics-inferred dynamics of {SARS}-{C}o{V}-2
                      interactions with host epithelial cells.},
      journal      = {Science signaling},
      volume       = {16},
      number       = {804},
      issn         = {1945-0877},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2023-01948},
      pages        = {eabl8266},
      year         = {2023},
      note         = {#LA:B330#},
      abstract     = {Virus-host interactions can reveal potentially effective
                      and selective therapeutic targets for treating infection.
                      Here, we performed an integrated analysis of the dynamics of
                      virus replication and the host cell transcriptional response
                      to severe acute respiratory syndrome coronavirus 2
                      (SARS-CoV-2) infection using human Caco-2 colon cancer cells
                      as a model. Time-resolved RNA sequencing revealed that, upon
                      infection, cells immediately transcriptionally activated
                      genes associated with inflammatory pathways that mediate the
                      antiviral response, which was followed by an increase in the
                      expression of genes involved in ribosome and mitochondria
                      function, thus suggesting rapid alterations in protein
                      production and cellular energy supply. At later stages,
                      between 24 and 48 hours after infection, the expression of
                      genes involved in metabolic processes-in particular, those
                      related to xenobiotic metabolism-was decreased. Mathematical
                      modeling incorporating SARS-CoV-2 replication suggested that
                      SARS-CoV-2 proteins inhibited the host antiviral response
                      and that virus transcripts exceeded the translation capacity
                      of the host cells. Targeting kinase-dependent pathways that
                      exhibited increases in transcription in host cells was as
                      effective as a virus-targeted inhibitor at repressing viral
                      replication. Our findings in this model system delineate a
                      sequence of SARS-CoV-2 virus-host interactions that may
                      facilitate the identification of druggable host pathways to
                      suppress infection.},
      cin          = {F140 / B330},
      ddc          = {500},
      cid          = {I:(DE-He78)F140-20160331 / I:(DE-He78)B330-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37751479},
      doi          = {10.1126/scisignal.abl8266},
      url          = {https://inrepo02.dkfz.de/record/283165},
}