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@ARTICLE{Rommel:181976,
      author       = {M. G. E. Rommel and L. Walz and F. Fotopoulou$^*$ and S.
                      Kohlscheen and F. Schenk and C. Miskey and L. Botezatu and
                      Y. Krebs and I. M. Voelker and K. Wittwer and T.
                      Holland-Letz$^*$ and Z. Ivics and V. von Messling and M. A.
                      G. Essers$^*$ and M. D. Milsom$^*$ and C. K. Pfaller and U.
                      Modlich},
      title        = {{I}nfluenza {A} virus infection instructs hematopoiesis to
                      megakaryocyte-lineage output.},
      journal      = {Cell reports},
      volume       = {41},
      number       = {1},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2022-02338},
      pages        = {111447},
      year         = {2022},
      abstract     = {Respiratory tract infections are among the deadliest
                      communicable diseases worldwide. Severe cases of viral lung
                      infections are often associated with a cytokine storm and
                      alternating platelet numbers. We report that hematopoietic
                      stem and progenitor cells (HSPCs) sense a non-systemic
                      influenza A virus (IAV) infection via inflammatory
                      cytokines. Irrespective of antiviral treatment or
                      vaccination, at a certain threshold of IAV titer in the
                      lung, CD41-positive hematopoietic stem cells (HSCs) enter
                      the cell cycle while endothelial protein C receptor-positive
                      CD41-negative HSCs remain quiescent. Active CD41-positive
                      HSCs represent the source of megakaryocytes, while their
                      multi-lineage reconstitution potential is reduced. This
                      emergency megakaryopoiesis is thrombopoietin independent and
                      attenuated in IAV-infected interleukin-1 receptor-deficient
                      mice. Newly produced platelets during IAV infection are
                      immature and hyper-reactive. After viral clearance, HSC
                      quiescence is re-established. Our study reveals that
                      non-systemic viral respiratory infection has an acute impact
                      on HSCs via inflammatory cytokines to counteract IAV-induced
                      thrombocytopenia.},
      keywords     = {CP: Immunology (Other) / CP: Microbiology (Other) /
                      cytokines (Other) / emergency megakaryopoiesis (Other) /
                      hematopoietic stem cell activation (Other) / inflammation
                      (Other) / influenza (Other) / platelet activation (Other) /
                      respiratory virus infection (Other) / vaccination (Other)},
      cin          = {A012 / C060 / A011},
      ddc          = {610},
      cid          = {I:(DE-He78)A012-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)A011-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36198277},
      doi          = {10.1016/j.celrep.2022.111447},
      url          = {https://inrepo02.dkfz.de/record/181976},
}