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10.1128/JVI.00990-09

http://scihub22266oqcxt.onion/10.1128/JVI.00990-09
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suck abstract from ncbi


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pmid19656886
      J+Virol 2009 ; 83 (20 ): 10406-16
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  • Cell entry of Borna disease virus follows a clathrin-mediated endocytosis pathway that requires Rab5 and microtubules #MMPMID19656886
  • Clemente R ; de la Torre JC
  • J Virol 2009[Oct]; 83 (20 ): 10406-16 PMID19656886 show ga
  • Borna disease virus (BDV), the prototypic member of the Bornaviridae family within the order Mononegavirales, exhibits high neurotropism and provides an important and unique experimental model system for studying virus-cell interactions within the central nervous system. BDV surface glycoprotein (G) plays a critical role in virus cell entry via receptor-mediated endocytosis, and therefore, G is a critical determinant of virus tissue and cell tropism. However, the specific cell pathways involved in BDV cell entry have not been determined. Here, we provide evidence that BDV uses a clathrin-mediated, caveola-independent cell entry pathway. We also show that BDV G-mediated fusion takes place at an optimal pH of 6.0 to 6.2, corresponding to an early-endosome compartment. Consistent with this finding, BDV cell entry was Rab5 dependent but Rab7 independent and exhibited rapid fusion kinetics. Our results also uncovered a key role for microtubules in BDV cell entry, whereas the integrity and dynamics of actin cytoskeleton were not required for efficient cell entry of BDV.
  • |*Endocytosis [MESH]
  • |*Host-Pathogen Interactions [MESH]
  • |Animals [MESH]
  • |Borna Disease/virology [MESH]
  • |Borna disease virus/genetics/metabolism/*pathogenicity [MESH]
  • |Cell Line [MESH]
  • |Chlorocebus aethiops [MESH]
  • |Clathrin/metabolism/pharmacology [MESH]
  • |Humans [MESH]
  • |Microtubules/*metabolism [MESH]
  • |Oligodendroglia/*virology [MESH]
  • |Vero Cells [MESH]
  • |Virus Internalization [MESH]


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