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@ARTICLE{Passos:267514,
      author       = {Passos, Vania and Henkel, Lisa M and Wang, Jiayi and
                      Zapatero-Belinchón, Francisco J and Möller, Rebecca and
                      Sun, Guorong and Waltl, Inken and Schneider, Talia and
                      Wachs, Amelie and Ritter, Birgit and Kropp, Kai A and Zhu,
                      Shuyong and Deleidi, Michela and Kalinke, Ulrich and Schulz,
                      Thomas F and Höglinger, Günter and Gerold, Gisa and
                      Wegner, Florian and Viejo-Borbolla, Abel},
      title        = {{I}nnate immune response to {SARS}-{C}o{V}-2 infection
                      contributes to neuronal damage in human i{PSC}-derived
                      peripheral neurons.},
      journal      = {Journal of medical virology},
      volume       = {96},
      number       = {2},
      issn         = {0146-6615},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley},
      reportid     = {DZNE-2024-00160},
      pages        = {e29455},
      year         = {2024},
      abstract     = {Severe acute respiratory coronavirus 2 (SARS-CoV-2) causes
                      neurological disease in the peripheral and central nervous
                      system (PNS and CNS, respectively) of some patients. It is
                      not clear whether SARS-CoV-2 infection or the subsequent
                      immune response are the key factors that cause neurological
                      disease. Here, we addressed this question by infecting human
                      induced pluripotent stem cell-derived CNS and PNS neurons
                      with SARS-CoV-2. SARS-CoV-2 infected a low number of CNS
                      neurons and did not elicit a robust innate immune response.
                      On the contrary, SARS-CoV-2 infected a higher number of PNS
                      neurons. This resulted in expression of interferon (IFN)
                      λ1, several IFN-stimulated genes and proinflammatory
                      cytokines. The PNS neurons also displayed alterations
                      characteristic of neuronal damage, as increased levels of
                      sterile alpha and Toll/interleukin receptor motif-containing
                      protein 1, amyloid precursor protein and α-synuclein, and
                      lower levels of cytoskeletal proteins. Interestingly,
                      blockade of the Janus kinase and signal transducer and
                      activator of transcription pathway by Ruxolitinib did not
                      increase SARS-CoV-2 infection, but reduced neuronal damage,
                      suggesting that an exacerbated neuronal innate immune
                      response contributes to pathogenesis in the PNS. Our results
                      provide a basis to study coronavirus disease 2019 (COVID-19)
                      related neuronal pathology and to test future preventive or
                      therapeutic strategies.},
      keywords     = {Humans / COVID-19 / Induced Pluripotent Stem Cells /
                      SARS-CoV-2 / Immunity, Innate / Neurons / JAK/STAT (Other) /
                      SARM1 (Other) / SARS-CoV-2 (Other) / iPSC-derived peripheral
                      neurons (Other) / interferon (Other) / neuronal damage
                      (Other)},
      cin          = {AG Deleidi},
      ddc          = {610},
      cid          = {I:(DE-2719)1210011},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38323709},
      doi          = {10.1002/jmv.29455},
      url          = {https://pub.dzne.de/record/267514},
}