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@ARTICLE{RybakWolf:277076,
      author       = {A. Rybak-Wolf and E. Wyler and T. M. Pentimalli and I.
                      Legnini and A. Oliveras Martinez and P. Glažar and A. Loewa
                      and S. J. Kim and B. B. Kaufer and A. Woehler and M.
                      Landthaler and N. Rajewsky$^*$},
      title        = {{M}odelling viral encephalitis caused by herpes simplex
                      virus 1 infection in cerebral organoids.},
      journal      = {Nature microbiology},
      volume       = {8},
      number       = {7},
      issn         = {2058-5276},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2023-01260},
      pages        = {1252-1266},
      year         = {2023},
      note         = {2023 Jul;8(7):1252-1266},
      abstract     = {Herpes simplex encephalitis is a life-threatening disease
                      of the central nervous system caused by herpes simplex
                      viruses (HSVs). Following standard of care with antiviral
                      acyclovir treatment, most patients still experience various
                      neurological sequelae. Here we characterize HSV-1 infection
                      of human brain organoids by combining single-cell RNA
                      sequencing, electrophysiology and immunostaining. We
                      observed strong perturbations of tissue integrity, neuronal
                      function and cellular transcriptomes. Under acyclovir
                      treatment viral replication was stopped, but did not prevent
                      HSV-1-driven defects such as damage of neuronal processes
                      and neuroepithelium. Unbiased analysis of pathways
                      deregulated upon infection revealed tumour necrosis factor
                      activation as a potential causal factor. Combination of
                      anti-inflammatory drugs such as necrostatin-1 or bardoxolone
                      methyl with antiviral treatment prevented the damages caused
                      by infection, indicating that tuning the inflammatory
                      response in acute infection may improve current therapeutic
                      strategies.},
      cin          = {BE01},
      ddc          = {570},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37349587},
      doi          = {10.1038/s41564-023-01405-y},
      url          = {https://inrepo02.dkfz.de/record/277076},
}