title: Classical swine fever virus failed to activate nuclear factor-kappa b signaling pathway both in vitro and in vivo.
abstract: BACKGROUND
  Classical swine fever virus (CSFV) is the cause of CSF which is a severe disease of pigs, leading to heavy economic losses in many regions of the world. Nuclear factor-kappa B (NF-κB) is a critical regulator of innate and adaptive immunity, and commonly activated upon viral infection. In our previous study, we found that CSFV could suppress the maturation and modulate the functions of monocyte-derived dendritic cells (Mo-DCs) without activating NF-κB pathway. To further prove the effects of CSFV on the NF-κB signaling pathway, we investigated the activity of NF-κB after CSFV infection in vivo and in vitro.
  
  
  METHODS
  Attenuated Thiverval strain and virulent wild-type GXW-07 strain were used as challenge viruses in this study. Porcine kidney 15 (PK-15) cells were cultured in vitro and peripheral blood mononuclear cells (PBMCs) were isolated from the blood of CSFV-infected pigs. DNA binding of NF-κB was measured by electrophoretic mobility shift assays (EMSA), NF-κB p65 translocation was detected using immunofluorescent staining, and p65/RelA and IκBα expression was measured by Western Blotting.
  
  
  RESULTS
  Infection of cells with CSFV in vitro and in vivo showed that compared with tumor necrosis factor alpha (TNF-α) stimulated cells, there was no distinct DNA binding band of NF-κB, and no significant translocation of p65/RelA from the cytoplasm to the nucleus was observed, which might have been due to the apparent lack of IkBa degradation.
  
  
  CONCLUSIONS
  CSFV infection had no effect on the NF-κB signaling pathway, indicating that CSFV could evade host activation of NF-κB during infection.
authors.affiliation: College of Veterinary Medicine, South China Agricultural University, 483 Wu Shan Road, Guangzhou, Tian He District 510642, China.
authors.forename: Li-Jun
authors.initials: LJ
authors.lastname: Chen
authors.forename: Xiao-Ying
authors.initials: XY
authors.lastname: Dong
authors.forename: Ming-Qiu
authors.initials: MQ
authors.lastname: Zhao
authors.forename: Hai-Yan
authors.initials: HY
authors.lastname: Shen
authors.forename: Jia-Ying
authors.initials: JY
authors.lastname: Wang
authors.forename: Jing-Jing
authors.initials: JJ
authors.lastname: Pei
authors.forename: Wen-Jun
authors.initials: WJ
authors.lastname: Liu
authors.forename: Yong-Wen
authors.initials: YW
authors.lastname: Luo
authors.forename: Chun-Mei
authors.initials: CM
authors.lastname: Ju
authors.forename: Jin-Ding
authors.initials: JD
authors.lastname: Chen
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D006691:Classical Swine Fever / Q000235:genetics / Q000276:immunology* / Q000821:virology*; D006692:Classical Swine Fever Virus / Q000276:immunology / Q000502:physiology*; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008025:Ligases / Q000235:genetics / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013552:Swine; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D016328:NF-kappa B; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D008025:Ligases; C028812:guanosine 3',5'-polyphosphate synthetases