The activation of the IFN beta induction/signaling pathway in porcine alveolar macrophages by porcine reproductive and respiratory syndrome virus is variable

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dc.contributor.authorOverend, Christopher C.en
dc.contributor.authorCui, Junruen
dc.contributor.authorGrubman, Marvin J.en
dc.contributor.authorGarmendia, Antonio E.en
dc.date.accessioned2020-03-26T13:00:33Zen
dc.date.available2020-03-26T13:00:33Zen
dc.date.issued2017-03en
dc.description.abstractBackground It has been recognized that the expression of type I interferon (IFN alpha/beta) may be suppressed during infection with porcine reproductive, respiratory syndrome virus (PRRSV). This causes profound negative effects on both the innate and adaptive immunity of the host resulting in persistence of infection. Objective Test the effects of PRRSV infection of porcine alveolar macrophages (PAMs), the main target cell, on the expression of interferon beta (IFN beta) and downstream signaling events. Methods In order to examine those effects, PAMs harvested from lungs of healthy PRRSV-free animals were infected with virulent, attenuated, infectious clone-derived chimeric viruses, or field PRRS virus strains. Culture supernatants from the infected PAMs were tested for IFN beta protein expression by means of indirect ELISA and for bioactivity by a vesicular stomatitis virus plaque reduction assay. The expression of the Mx protein was assayed to ascertain signaling events. Results These experiments demonstrated that PRRSV does induce variably, the expression of bioactive IFN beta protein in the natural host cell. To further elucidate the effects of PRRSV infection on IFN beta signaling, Mx-1 an interferon stimulated gene (ISG), was also tested for expression. Interestingly, Mx-1 expression by infected PAMs generally correlated with IFN beta production. Conclusion The results of this study demonstrate that the induction of IFN beta and signaling in PAMs after PRRSV infection is variable.en
dc.description.adminPublic domain – authored by a U.S. government employeeen
dc.description.notesThis work was supported by funds from the Specific Cooperative Agreement #58-1940-2-245 between the University of Connecticut and the USDA, ARS, USDA grant # 20043520414267, Integrated Control and Elimination of PRRS (NC229), Storrs Agricultural Experiment Station, University of Connecticut. The authors thank Drs. F. Osorio and A. Pattnaik (University of Nebraska, Lincoln, NE) for providing the chimeric viruses used in this work. The authors also thank Dr. Surya Waghela (Texas A&M University, College Station, TX) for valuable suggestions with the manuscript.en
dc.description.sponsorshipUniversity of Connecticut [58-1940-2-245]; USDAUnited States Department of Agriculture (USDA) [58-1940-2-245]; Integrated Control and Elimination of PRRS [NC229]; Storrs Agricultural Experiment Station, University of Connecticut; ARS, USDAUnited States Department of Agriculture (USDA) [20043520414267]en
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1007/s11259-016-9665-6en
dc.identifier.eissn1573-7446en
dc.identifier.issn0165-7380en
dc.identifier.issue1en
dc.identifier.pmid27896670en
dc.identifier.urihttp://hdl.handle.net/10919/97488en
dc.identifier.volume41en
dc.language.isoenen
dc.rightsCreative Commons CC0 1.0 Universal Public Domain Dedicationen
dc.rights.urihttp://creativecommons.org/publicdomain/zero/1.0/en
dc.subjectPorcine reproductive respiratory syndrome virusen
dc.subjectInterferon betaen
dc.subjectMx-1 innate immunityen
dc.titleThe activation of the IFN beta induction/signaling pathway in porcine alveolar macrophages by porcine reproductive and respiratory syndrome virus is variableen
dc.title.serialVeterinary Research Communicationsen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.dcmitypeStillImageen

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