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Title: Porcine circovirus type 2 induces the activation of nuclear factor kappa B by I{kappa}B{alpha} degradation

Abstract

The transcription factor NF-{kappa}B 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-{kappa}B in PCV2-infected PK15 cells. In PCV2-infected cells, NF-{kappa}B was activated concomitantly with viral replication, which was characterized by increased DNA binding activity, translocation of NF-{kappa}B p65 from the cytoplasm to the nucleus, as well as degradation and phosphorylation of I{kappa}B{alpha} protein. We further demonstrated PCV2-induced activation of NF-{kappa}B and colocalization of p65 nuclear translocation with virus replication in cultured cells. Treatment of cells with CAPE, a selective inhibitor of NF-{kappa}B 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-{kappa}B 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.

Authors:
 [1];  [2]; ; ; ;  [1]
  1. Institute of Animal Husbandry and Veterinary Medicine, Beijing Municipal Academy of Agriculture and Forestry Sciences, No.9 Shuguang Garden Central Road, Haidian District, Beijing 100097 (China)
  2. Animal Health Biotechnology Group, Temasek Life Sciences Laboratory, National University of Singapore, 1 Research Link, Singapore 117604 (Singapore)
Publication Date:
OSTI Identifier:
21141030
Resource Type:
Journal Article
Journal Name:
Virology
Additional Journal Information:
Journal Volume: 378; Journal Issue: 1; Other Information: DOI: 10.1016/j.virol.2008.05.013; PII: S0042-6822(08)00340-1; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0042-6822
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; CYTOPLASM; DNA; PHOSPHORYLATION; SWINE; TRANSCRIPTION FACTORS; TRANSLOCATION; VIRUSES

Citation Formats

Li, Wei, Kwang, Jimmy, Jin, Wang, Lei, Shi, Bing, Yang, Yongqing, Li, and Liu Jue. Porcine circovirus type 2 induces the activation of nuclear factor kappa B by I{kappa}B{alpha} degradation. United States: N. p., 2008. Web. doi:10.1016/j.virol.2008.05.013.
Li, Wei, Kwang, Jimmy, Jin, Wang, Lei, Shi, Bing, Yang, Yongqing, Li, & Liu Jue. Porcine circovirus type 2 induces the activation of nuclear factor kappa B by I{kappa}B{alpha} degradation. United States. https://doi.org/10.1016/j.virol.2008.05.013
Li, Wei, Kwang, Jimmy, Jin, Wang, Lei, Shi, Bing, Yang, Yongqing, Li, and Liu Jue. 2008. "Porcine circovirus type 2 induces the activation of nuclear factor kappa B by I{kappa}B{alpha} degradation". United States. https://doi.org/10.1016/j.virol.2008.05.013.
@article{osti_21141030,
title = {Porcine circovirus type 2 induces the activation of nuclear factor kappa B by I{kappa}B{alpha} degradation},
author = {Li, Wei and Kwang, Jimmy and Jin, Wang and Lei, Shi and Bing, Yang and Yongqing, Li and Liu Jue},
abstractNote = {The transcription factor NF-{kappa}B 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-{kappa}B in PCV2-infected PK15 cells. In PCV2-infected cells, NF-{kappa}B was activated concomitantly with viral replication, which was characterized by increased DNA binding activity, translocation of NF-{kappa}B p65 from the cytoplasm to the nucleus, as well as degradation and phosphorylation of I{kappa}B{alpha} protein. We further demonstrated PCV2-induced activation of NF-{kappa}B and colocalization of p65 nuclear translocation with virus replication in cultured cells. Treatment of cells with CAPE, a selective inhibitor of NF-{kappa}B 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-{kappa}B 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.},
doi = {10.1016/j.virol.2008.05.013},
url = {https://www.osti.gov/biblio/21141030}, journal = {Virology},
issn = {0042-6822},
number = 1,
volume = 378,
place = {United States},
year = {Fri Aug 15 00:00:00 EDT 2008},
month = {Fri Aug 15 00:00:00 EDT 2008}
}