PMID- 16129468
OWN - NLM
STAT- MEDLINE
DCOM- 20051223
LR  - 20200403
IS  - 0042-6822 (Print)
IS  - 1096-0341 (Electronic)
IS  - 0042-6822 (Linking)
VI  - 342
IP  - 1
DP  - 2005 Nov 10
TI  - Porcine arterivirus activates the NF-kappaB pathway through IkappaB degradation.
PG  - 47-59
AB  - Nuclear factor-kappaB (NF-kappaB) is a critical regulator of innate and adaptive 
      immune function as well as cell proliferation and survival. The present study 
      demonstrated for the first time that a virus belonging to the Arteriviridae 
      family activates NF-kappaB in MARC-145 cells and alveolar macrophages. In porcine 
      reproductive and respiratory syndrome virus (PRRSV)-infected cells, NF-kappaB 
      activation was characterized by translocation of NF-kappaB from the cytoplasm to 
      the nucleus, increased DNA binding activity, and NF-kappaB-regulated gene 
      expression. NF-kappaB activation was increased as PRRSV infection progressed and 
      in a viral dose-dependent manner. UV-inactivation of PRRSV significantly reduced 
      the level of NF-kappaB activation. Degradation of IkappaB protein was detected 
      late in PRRSV infection, and overexpression of the dominant negative form of 
      IkappaBalpha (IkappaBalphaDN) significantly suppressed NF-kappaB activation 
      induced by PRRSV. However, IkappaBalphaDN did not affect viral replication and 
      viral cytopathic effect. PRRSV infection induced oxidative stress in cells by 
      generating reactive oxygen species (ROS), and antioxidants inhibited NF-kappaB 
      DNA binding activity in PRRSV-infected cells, suggesting ROS as a mechanism by 
      which NF-kappaB was activated by PRRSV infection. Moreover, NF-kappaB-dependent 
      expression of matrix metalloproteinase (MMP)-2 and MMP-9 was observed in 
      PRRSV-infected cells, an observation which implies that NF-kappaB activation is a 
      biologically significant aspect of PRRSV pathogenesis. The results presented here 
      provide a basis for understanding molecular pathways of pathology and immune 
      evasion associated with disease caused by PRRSV.
FAU - Lee, Sang-Myeong
AU  - Lee SM
AD  - Department of Veterinary Pathobiology, College of Veterinary Medicine, University 
      of Missouri-Columbia, MO 65211, USA.
FAU - Kleiboeker, Steven B
AU  - Kleiboeker SB
LA  - eng
PT  - Journal Article
DEP - 20050829
PL  - United States
TA  - Virology
JT  - Virology
JID - 0110674
RN  - 0 (I-kappa B Proteins)
RN  - 0 (NF-kappa B)
RN  - 9007-49-2 (DNA)
RN  - EC 1.13.12.- (Luciferases)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Active Transport, Cell Nucleus
MH  - Animals
MH  - Base Sequence
MH  - Cell Line
MH  - Cells, Cultured
MH  - DNA/genetics/metabolism
MH  - Gene Expression Regulation
MH  - Genes, Reporter
MH  - Humans
MH  - I-kappa B Proteins/*metabolism
MH  - Luciferases/genetics
MH  - Macrophages, Alveolar/metabolism/microbiology/virology
MH  - Matrix Metalloproteinase 2/genetics/metabolism
MH  - Matrix Metalloproteinase 9/genetics/metabolism
MH  - NF-kappa B/*metabolism
MH  - Oxidative Stress
MH  - Porcine respiratory and reproductive syndrome 
      virus/immunology/*pathogenicity/physiology
MH  - Swine
MH  - Virus Replication
PMC - PMC7111765
EDAT- 2005/09/01 09:00
MHDA- 2005/12/24 09:00
PMCR- 2005/08/29
CRDT- 2005/09/01 09:00
PHST- 2005/04/11 00:00 [received]
PHST- 2005/05/25 00:00 [revised]
PHST- 2005/07/29 00:00 [accepted]
PHST- 2005/09/01 09:00 [pubmed]
PHST- 2005/12/24 09:00 [medline]
PHST- 2005/09/01 09:00 [entrez]
PHST- 2005/08/29 00:00 [pmc-release]
AID - S0042-6822(05)00452-6 [pii]
AID - 10.1016/j.virol.2005.07.034 [doi]
PST - ppublish
SO  - Virology. 2005 Nov 10;342(1):47-59. doi: 10.1016/j.virol.2005.07.034. Epub 2005 
      Aug 29.