Please use this identifier to cite or link to this item:
|Title:||Porcine circovirus type 2 induces the activation of nuclear factor kappa B by IκBα degradation||Authors:||Wei, L.
|Issue Date:||2008||Citation:||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.||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
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Mar 6, 2018
WEB OF SCIENCETM
checked on Dec 24, 2018
checked on Apr 21, 2019
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.