title: The activation of the IFNβ induction/signaling pathway in porcine alveolar macrophages by porcine reproductive and respiratory syndrome virus is variable.
abstract: BACKGROUND
  It has been recognized that the expression of type I interferon (IFNα/β) 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 (IFNβ) 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 IFNβ 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 IFNβ protein in the natural host cell. To further elucidate the effects of PRRSV infection on IFNβ signaling, Mx-1 an interferon stimulated gene (ISG), was also tested for expression. Interestingly, Mx-1 expression by infected PAMs generally correlated with IFNβ production.
  
  
  CONCLUSIONS
  The results of this study demonstrate that the induction of IFNβ and signaling in PAMs after PRRSV infection is variable.
authors.affiliation: Department of Pathobiology and Veterinary Science, University of Connecticut, 61 North Eagleville Rd, Storrs, CT, 06269, USA.|Department of Biomedical Sciences and Pathobiology Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, 1981 Kraft Drive, Blacksburg, VA, 24061-0913, USA.
authors.forename: Christopher C
authors.initials: CC
authors.lastname: Overend
authors.affiliation: Department of Pathobiology and Veterinary Science, University of Connecticut, 61 North Eagleville Rd, Storrs, CT, 06269, USA.
authors.forename: Junru
authors.initials: J
authors.lastname: Cui
authors.affiliation: Plum Island Animal Disease Center,USDA/ARS, Greenport, NY, USA.
authors.forename: Marvin J
authors.initials: MJ
authors.lastname: Grubman
authors.affiliation: Department of Pathobiology and Veterinary Science, University of Connecticut, 61 North Eagleville Rd, Storrs, CT, 06269, USA. Antonio.Garmendia@uconn.edu.
authors.forename: Antonio E
authors.initials: AE
authors.lastname: Garmendia
mesh_terms: D000818:Animals; D004797:Enzyme-Linked Immunosorbent Assay; D005786:Gene Expression Regulation / Q000276:immunology; D054884:Host-Pathogen Interactions; D016899:Interferon-beta / Q000235:genetics* / Q000378:metabolism; D008168:Lung / Q000821:virology; D016676:Macrophages, Alveolar / Q000276:immunology* / Q000821:virology; D064547:Myxovirus Resistance Proteins / Q000235:genetics; D019318:Porcine Reproductive and Respiratory Syndrome / Q000276:immunology*; D019316:Porcine respiratory and reproductive syndrome virus / Q000276:immunology*; D015398:Signal Transduction; D013552:Swine
chemical_list: D064547:Myxovirus Resistance Proteins; D016899:Interferon-beta
keywords: Interferon beta; Mx-1 innate immunity; Porcine reproductive respiratory syndrome virus