PMID- 15507307
OWN - NLM
STAT- MEDLINE
DCOM- 20041229
LR  - 20200407
IS  - 0165-2427 (Print)
IS  - 1873-2534 (Electronic)
IS  - 0165-2427 (Linking)
VI  - 102
IP  - 3
DP  - 2004 Dec 8
TI  - Porcine reproductive and respiratory syndrome virus field isolates differ in in 
      vitro interferon phenotypes.
PG  - 217-31
AB  - Type I interferons (IFN-alpha and -beta) play an important role in the innate 
      host defense against viral infection by inducing antiviral responses. In addition 
      to direct antiviral activities, type I IFN serves as an important link between 
      the innate and adaptive immune response through multiple mechanisms. Therefore, 
      the outcome of a viral infection can be affected by IFN induction and the IFN 
      sensitivity of a virus. North American porcine reproductive and respiratory 
      syndrome virus (PRRSV) field isolates were studied with regard to IFN-alpha 
      sensitivity and induction in order to understand the role of type I IFN in PRRSV 
      pathogenesis. PRRSV isolates were differentially sensitive to porcine recombinant 
      IFN-alpha (rIFN-alpha) and varied in their ability to induce IFN-alpha in porcine 
      alveolar macrophages (PAM) cultures as measured by a porcine IFN-alpha specific 
      ELISA on cell culture supernatants. Fifty-two plaques were purified from three 
      PRRSV isolates (numbers 3, 7, and 12) and tested for IFN sensitivity and IFN 
      induction. Plaque-derived populations were composed of heterogeneous populations 
      in terms of IFN-inducing capacity and sensitivity to rIFN-alpha. When macrophages 
      infected with isolates 3, 7, or 12 were treated with polycytidylic acid 
      (polyI:C), IFN-alpha production was enhanced. Cells infected with isolate 3 and 
      treated with polyI:C showed the most consistent and strongest enhancement of 
      IFN-alpha production. It was demonstrated that the relatively low concentrations 
      of IFN-alpha produced by isolate 3 contributed to the enhanced IFN-alpha 
      synthesis in response to polyI:C. Isolates 7 and 12 significantly suppressed the 
      enhanced IFN-alpha production by isolate 3 in polyI:C treated cells. To determine 
      if suppression was at the level of IFN-alpha transcription, quantitative RT-PCR 
      was performed for IFN-alpha mRNA and compared to GAPDH and cyclophilin mRNA 
      quantification. However, the relative number of IFN-alpha transcript copies did 
      not correlate with IFN-alpha protein levels, suggesting a post-transcriptional 
      mechanism of suppression. In summary, these results demonstrate that PRRSV field 
      isolates differ both in IFN-alpha sensitivity and induction. Furthermore, a PRRSV 
      field isolate strongly enhance polyI:C-induced IFN-alpha production in PAM 
      cultures and this priming effect was suppressed by other PRRSV isolates.
FAU - Lee, Sang-Myeong
AU  - Lee SM
AD  - Department of Veterinary Pathobiology, College of Veterinary Medicine, University 
      of Missouri, 1600 E. Rollins, Columbia, MO 65211, USA.
FAU - Schommer, Susan K
AU  - Schommer SK
FAU - Kleiboeker, Steven B
AU  - Kleiboeker SB
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Vet Immunol Immunopathol
JT  - Veterinary immunology and immunopathology
JID - 8002006
RN  - 0 (Interferon-alpha)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Cells, Cultured
MH  - Chlorocebus aethiops
MH  - Genetic Variation
MH  - Interferon-alpha/biosynthesis/*immunology
MH  - Macrophages, Alveolar
MH  - Phenotype
MH  - Porcine Reproductive and Respiratory Syndrome/virology
MH  - Porcine respiratory and reproductive syndrome virus/drug 
      effects/genetics/*immunology
MH  - Swine/immunology/virology
MH  - Time Factors
PMC - PMC7112598
EDAT- 2004/10/28 09:00
MHDA- 2004/12/30 09:00
PMCR- 2004/10/13
CRDT- 2004/10/28 09:00
PHST- 2004/10/28 09:00 [pubmed]
PHST- 2004/12/30 09:00 [medline]
PHST- 2004/10/28 09:00 [entrez]
PHST- 2004/10/13 00:00 [pmc-release]
AID - S0165-2427(04)00255-7 [pii]
AID - 10.1016/j.vetimm.2004.09.009 [doi]
PST - ppublish
SO  - Vet Immunol Immunopathol. 2004 Dec 8;102(3):217-31. doi: 
      10.1016/j.vetimm.2004.09.009.