PMID- 15936905
OWN - NLM
STAT- MEDLINE
DCOM- 20050817
LR  - 20220316
IS  - 0378-1135 (Print)
IS  - 1873-2542 (Electronic)
IS  - 0378-1135 (Linking)
VI  - 108
IP  - 3-4
DP  - 2005 Jul 1
TI  - Reduction of porcine reproductive and respiratory syndrome virus (PRRSV) 
      infection in swine alveolar macrophages by porcine circovirus 2 (PCV2)-induced 
      interferon-alpha.
PG  - 167-77
AB  - Two common viral pathogens of swine, namely, porcine circovirus type 2 (PCV2) and 
      porcine reproductive and respiratory syndrome virus (PRRSV), were investigated in 
      regard to their effects on monolayer cultures of swine alveolar macrophages 
      (AMs). The purpose was to identify selected cellular changes and responses 
      potentially associated with the clinical reactions of pigs infected with either 
      or both of these viruses. Measurements included the (1) absolute and relative 
      numbers of infected, viable, and apoptotic cells; (2) distribution of viral 
      antigens; (3) levels of interferon-alpha (IFN-alpha) and tumor necrosis 
      factor-alpha (TNF-alpha) produced and their association with the extent of 
      virus-induced cytopathology. Four groups of AMs were studied, including 
      mock-infected, PCV2 alone-infected (PCV2-A), PRRSV alone-infected (PRRSV-A), and 
      PCV2 and PRRSV dually infected (PCV2/PRRSV) groups. The AMs of PCV2-A group had 
      high antigen-containing rate without cell death. There was a marked increase in 
      cell death and apoptosis in PRRSV-A group. However, a lower PRRSV-induced 
      infectious rate, cell death, and apoptosis were seen in PCV2/PRRSV group. High 
      levels of IFN-alpha production were detected in PCV2-infected groups, but not in 
      mock-infected and PRRSV-A groups. The PRRSV-induced cytopathic effect (CPE) on 
      MARC-145 cells or swine AMs was markedly reduced by pre-incubation of the cells 
      with UV-treated or non-UV-treated supernatants of PCV2-infected AMs. In addition, 
      the reduction in CPE was abolished when the supernatants of PCV2-infected AMs 
      were pre-treated with a mouse anti-recombinant porcine IFN-alpha antibody. The 
      results suggest that swine AMs were an important reservoir of PCV2; PCV2 
      infection reduced PRRSV infection and PRRSV-associated CPE in PCV2/PRRSV AMs; the 
      reduction of PRRSV infection in AMs was mediated by IFN-alpha generated by PCV2 
      infection. The reduced PRRSV-associated CPE in AMs and increased pro-inflammatory 
      cytokine production may lead to a more severe pneumonic lesion in those dually 
      infected pigs.
FAU - Chang, Hui-Wen
AU  - Chang HW
AD  - Graduate Institute of Veterinary Medicine, National Taiwan University, Taipei 
      106, Taiwan, ROC.
FAU - Jeng, Chian-Ren
AU  - Jeng CR
FAU - Liu, Jiuan J
AU  - Liu JJ
FAU - Lin, Tsang-Long
AU  - Lin TL
FAU - Chang, Chih-Cheng
AU  - Chang CC
FAU - Chia, Mi-Yuan
AU  - Chia MY
FAU - Tsai, Yi-Chieh
AU  - Tsai YC
FAU - Pang, Victor F
AU  - Pang VF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Vet Microbiol
JT  - Veterinary microbiology
JID - 7705469
RN  - 0 (Antibodies, Viral)
RN  - 0 (Antigens, Viral)
RN  - 0 (Interferon-alpha)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antibodies, Viral/immunology
MH  - Antigens, Viral/analysis
MH  - Apoptosis/immunology
MH  - Biological Assay/veterinary
MH  - Circoviridae Infections/complications/*immunology/virology
MH  - Circovirus/*immunology
MH  - Cytopathogenic Effect, Viral/immunology
MH  - Female
MH  - Fluorescent Antibody Technique/veterinary
MH  - Interferon-alpha/biosynthesis/*immunology
MH  - Macrophages, Alveolar/*immunology/virology
MH  - Male
MH  - Porcine Reproductive and Respiratory Syndrome/*immunology/virology
MH  - Porcine respiratory and reproductive syndrome virus/*immunology
MH  - Specific Pathogen-Free Organisms
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/immunology
PMC - PMC7117408
EDAT- 2005/06/07 09:00
MHDA- 2005/08/18 09:00
PMCR- 2005/06/03
CRDT- 2005/06/07 09:00
PHST- 2004/11/03 00:00 [received]
PHST- 2005/03/09 00:00 [revised]
PHST- 2005/03/17 00:00 [accepted]
PHST- 2005/06/07 09:00 [pubmed]
PHST- 2005/08/18 09:00 [medline]
PHST- 2005/06/07 09:00 [entrez]
PHST- 2005/06/03 00:00 [pmc-release]
AID - S0378-1135(05)00116-1 [pii]
AID - 10.1016/j.vetmic.2005.03.010 [doi]
PST - ppublish
SO  - Vet Microbiol. 2005 Jul 1;108(3-4):167-77. doi: 10.1016/j.vetmic.2005.03.010.