Source:http://linkedlifedata.com/resource/pubmed/id/15507307
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2004-10-27
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| pubmed:abstractText |
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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Dec
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| pubmed:issn |
0165-2427
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
8
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| pubmed:volume |
102
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
217-31
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:15507307-Animals,
pubmed-meshheading:15507307-Cell Line,
pubmed-meshheading:15507307-Cells, Cultured,
pubmed-meshheading:15507307-Cercopithecus aethiops,
pubmed-meshheading:15507307-Genetic Variation,
pubmed-meshheading:15507307-Interferon-alpha,
pubmed-meshheading:15507307-Macrophages, Alveolar,
pubmed-meshheading:15507307-Phenotype,
pubmed-meshheading:15507307-Porcine Reproductive and Respiratory Syndrome,
pubmed-meshheading:15507307-Porcine respiratory and reproductive syndrome virus,
pubmed-meshheading:15507307-Swine,
pubmed-meshheading:15507307-Time Factors
|
| pubmed:year |
2004
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| pubmed:articleTitle |
Porcine reproductive and respiratory syndrome virus field isolates differ in in vitro interferon phenotypes.
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| pubmed:affiliation |
Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri, 1600 E. Rollins, Columbia, MO 65211, USA.
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| pubmed:publicationType |
Journal Article
|