Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.virol.2008.05.013
Title: Porcine circovirus type 2 induces the activation of nuclear factor kappa B by IκBα degradation
Authors: Wei, L.
Wang, J.
Shi, L.
Yang, B.
Li, Y.
Liu, J.
Kwang, J. 
Keywords: Caspase-3 activity
IκB family
NF-κB
PCV2
PK15 cells
Issue Date: 2008
Source: Wei, L., Wang, J., Shi, L., Yang, B., Li, Y., Liu, J., Kwang, J. (2008). Porcine circovirus type 2 induces the activation of nuclear factor kappa B by IκBα degradation. Virology 378 (1) : 177-184. ScholarBank@NUS Repository. https://doi.org/10.1016/j.virol.2008.05.013
Abstract: The transcription factor NF-κB is commonly activated upon virus infection and a key player in the induction and regulation of the host immune response. The present study demonstrated for the first time that porcine circovirus type 2 (PCV2), which is the primary causative agent of an emerging swine disease, postweaning multisystemic wasting syndrome, can activate NF-κB in PCV2-infected PK15 cells. In PCV2-infected cells, NF-κB was activated concomitantly with viral replication, which was characterized by increased DNA binding activity, translocation of NF-κB p65 from the cytoplasm to the nucleus, as well as degradation and phosphorylation of IκBα protein. We further demonstrated PCV2-induced activation of NF-κB and colocalization of p65 nuclear translocation with virus replication in cultured cells. Treatment of cells with CAPE, a selective inhibitor of NF-κB activation, reduced virus protein expression and progeny production followed by decreasing PCV2-induced apoptotic caspase activity, indicating the involvement of this transcription factor in induction of cell death. Taken together, these data suggest that NF-κB activation is important for PCV2 replication and contributes to virus-mediated changes in host cells. The results presented here provide a basis for understanding molecular mechanism of PCV2 infection. © 2008 Elsevier Inc. All rights reserved.
Source Title: Virology
URI: http://scholarbank.nus.edu.sg/handle/10635/24761
ISSN: 00426822
10960341
DOI: 10.1016/j.virol.2008.05.013
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