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@ARTICLE{Reis:178605,
      author       = {V. P. D. Reis and M. Keller and K. Schmidt$^*$ and R. G.
                      Ulrich and M. H. Groschup},
      title        = {α{V}β3 {I}ntegrin {E}xpression {I}s {E}ssential for
                      {R}eplication of {M}osquito and {T}ick-{B}orne
                      {F}laviviruses in {M}urine {F}ibroblast {C}ells.},
      journal      = {Viruses},
      volume       = {14},
      number       = {1},
      issn         = {1999-4915},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2022-00154},
      pages        = {18},
      year         = {2022},
      abstract     = {The Flavivirus genus includes a number of important viruses
                      that are pathogenic to humans and animals and are
                      responsible for outbreaks across the globe. Integrins, a
                      family of heterodimeric transmembrane molecules expressed in
                      all nucleated cells mediate critical functions of cell
                      physiology and cell cycle. Integrins were previously
                      postulated to be involved in flavivirus entry and to
                      modulate flavivirus replication efficiency. In the present
                      study, mouse embryonic fibroblasts (MEF), lacking the
                      expression of αVβ3 integrin (MEF-αVβ3-/-), were infected
                      with four different flaviviruses, namely yellow fever virus
                      (YFV), West Nile virus (WNV), Usutu virus (USUV) and Langat
                      virus (LGTV). The effects of the αVβ3 integrin absence in
                      double-knockout MEF-αVβ3-/- on flavivirus binding,
                      internalization and replication were compared to the
                      respective wild-type cells. Binding to the cell surface for
                      all four flaviviruses was not affected by the ablation of
                      αVβ3 integrin, whereas internalization of USUV and WNV was
                      slightly affected by the loss of αVβ3 integrin expression.
                      Most interestingly, the deletion of αVβ3 integrin strongly
                      impaired replication of all flaviviruses with a reduction of
                      up to $99\%$ on virus yields and a strong reduction on
                      flavivirus anti-genome RNA synthesis. In conclusion, our
                      results demonstrate that αVβ3 integrin expression in
                      flavivirus-susceptible cell lines enhances the flavivirus
                      replication.},
      keywords     = {flavivirus (Other) / host cell factors (Other) / integrins
                      (Other) / virus binding (Other) / virus internalization
                      (Other) / virus replication (Other)},
      cin          = {W440},
      ddc          = {050},
      cid          = {I:(DE-He78)W440-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35062222},
      doi          = {10.3390/v14010018},
      url          = {https://inrepo02.dkfz.de/record/178605},
}