Porcine reproductive and respiratory syndrome virus field isolates differ in in vitro interferon phenotypes
| Autor: | Sang-Myeong Lee, Steven B. Kleiboeker, Susan K. Schommer |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Alveolar macrophages
Time Factors Swine Immunology PAM porcine alveolar macrophages Porcine Reproductive and Respiratory Syndrome Biology Article Virus Cell Line law.invention Pathogenesis Interferon law Chlorocebus aethiops Macrophages Alveolar medicine Animals rIFN-α recombinant interferon-α Porcine respiratory and reproductive syndrome virus MOI multiplicity of infection Cells Cultured polyI:C polycytidylic acid General Veterinary p.i. post-infection TCID50 50% tissue culture infectious dose Genetic Variation Interferon-alpha Porcine reproductive and respiratory syndrome virus biology.organism_classification Acquired immune system Virology In vitro PRRSV porcine reproductive and respiratory syndrome virus Phenotype Cell culture Recombinant DNA Interferon-α medicine.drug |
| Zdroj: | Veterinary Immunology and Immunopathology |
| ISSN: | 0165-2427 |
| DOI: | 10.1016/j.vetimm.2004.09.009 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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