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10.1128/JVI.79.10.6043-6051.2005

http://scihub22266oqcxt.onion/10.1128/JVI.79.10.6043-6051.2005
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suck abstract from ncbi


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pmid15857990
      J+Virol 2005 ; 79 (10 ): 6043-51
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  • Constitutive activation of the transcription factor NF-kappaB results in impaired borna disease virus replication #MMPMID15857990
  • Bourteele S ; Oesterle K ; Pleschka S ; Unterstab G ; Ehrhardt C ; Wolff T ; Ludwig S ; Planz O
  • J Virol 2005[May]; 79 (10 ): 6043-51 PMID15857990 show ga
  • The inducible transcription factor NF-kappaB is commonly activated upon RNA virus infection and is a key player in the induction and regulation of the innate immune response. Borna disease virus (BDV) is a neurotropic negative-strand RNA virus, which replicates in the nucleus of the infected cell and causes a persistent infection that can lead to severe neurological disorders. To investigate the activation and function of NF-kappaB in BDV-infected cells, we stably transfected the highly susceptible neuronal guinea pig cell line CRL with a constitutively active (IKK EE) or dominant-negative (IKK KD) regulator of the IKK/NF-kappaB signaling pathway. While BDV titers were not affected in cells with impaired NF-kappaB signaling, the expression of an activated mutant of IkappaB kinase (IKK) resulted in a strong reduction in the intracellular viral titer in CRL cells. Electrophoretic mobility shift assays and luciferase reporter gene assays revealed that neither NF-kappaB nor interferon regulatory factors (IRFs) were activated upon acute BDV infection of wild-type or vector-transfected CRL cells. However, when IKK EE-transfected cells were used as target cells for BDV infection, DNA binding to an IRF3/7-responsive DNA element was detectable. Since IRF3/7 is a key player in the antiviral interferon response, our data indicate that enhanced NF-kappaB activity in the presence of BDV leads to the induction of antiviral pathways resulting in reduced virus titers. Consistent with this observation, the anti-BDV activity of NF-kappaB preferentially spread to areas of the brains of infected rats where activated NF-kappaB was not detectable.
  • |*Gene Expression Regulation, Viral [MESH]
  • |Animals [MESH]
  • |Borna Disease/metabolism/*virology [MESH]
  • |Borna disease virus/genetics/*physiology [MESH]
  • |Brain/metabolism [MESH]
  • |Cell Line [MESH]
  • |Female [MESH]
  • |Guinea Pigs [MESH]
  • |I-kappa B Kinase [MESH]
  • |Immunohistochemistry [MESH]
  • |NF-kappa B/*metabolism [MESH]
  • |Protein Serine-Threonine Kinases/metabolism [MESH]
  • |Rats [MESH]
  • |Signal Transduction [MESH]


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