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• W2016452561 abstract "Type I interferons (IFN-α and -β) 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-α 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-α (rIFN-α) and varied in their ability to induce IFN-α in porcine alveolar macrophages (PAM) cultures as measured by a porcine IFN-α 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-α. When macrophages infected with isolates 3, 7, or 12 were treated with polycytidylic acid (polyI:C), IFN-α production was enhanced. Cells infected with isolate 3 and treated with polyI:C showed the most consistent and strongest enhancement of IFN-α production. It was demonstrated that the relatively low concentrations of IFN-α produced by isolate 3 contributed to the enhanced IFN-α synthesis in response to polyI:C. Isolates 7 and 12 significantly suppressed the enhanced IFN-α production by isolate 3 in polyI:C treated cells. To determine if suppression was at the level of IFN-α transcription, quantitative RT-PCR was performed for IFN-α mRNA and compared to GAPDH and cyclophilin mRNA quantification. However, the relative number of IFN-α transcript copies did not correlate with IFN-α protein levels, suggesting a post-transcriptional mechanism of suppression. In summary, these results demonstrate that PRRSV field isolates differ both in IFN-α sensitivity and induction. Furthermore, a PRRSV field isolate strongly enhance polyI:C-induced IFN-α production in PAM cultures and this priming effect was suppressed by other PRRSV isolates." @default.
• W2016452561 created "2016-06-24" @default.
• W2016452561 creator A5003349249 @default.
• W2016452561 creator A5081266753 @default.
• W2016452561 creator A5082336809 @default.
• W2016452561 date "2004-12-01" @default.
• W2016452561 modified "2023-09-27" @default.
• W2016452561 title "Porcine reproductive and respiratory syndrome virus field isolates differ in in vitro interferon phenotypes" @default.
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• W2016452561 doi "https://doi.org/10.1016/j.vetimm.2004.09.009" @default.
• W2016452561 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7112598" @default.
• W2016452561 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15507307" @default.
• W2016452561 hasPublicationYear "2004" @default.
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