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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 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.