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      Porcine reproductive and respiratory syndrome (PRRS): an immune dysregulatory pandemic

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          Abstract

          Porcine reproductive and respiratory disease syndrome (PRRS) is a viral pandemic that especially affects neonates within the “critical window” of immunological development. PRRS was recognized in 1987 and within a few years became pandemic causing an estimated yearly $600,000 economic loss in the USA with comparative losses in most other countries. The causative agent is a single-stranded, positive-sense enveloped arterivirus (PRRSV) that infects macrophages and plasmacytoid dendritic cells. Despite the discovery of PRRSV in 1991 and the publication of >2,000 articles, the control of PRRS is problematic. Despite the large volume of literature on this disease, the cellular and molecular mechanisms describing how PRRSV dysregulates the host immune system are poorly understood. We know that PRRSV suppresses innate immunity and causes abnormal B cell proliferation and repertoire development, often lymphopenia and thymic atrophy. The PRRSV genome is highly diverse, rapidly evolving but amenable to the generation of many mutants and chimeric viruses for experimental studies. PRRSV only replicates in swine which adds to the experimental difficulty since no inbred well-defined animal models are available. In this article, we summarize current knowledge and apply it toward developing a series of provocative and testable hypotheses to explain how PRRSV immunomodulates the porcine immune system with the goal of adding new perspectives on this disease.

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          Most cited references208

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          Assessment of the economic impact of porcine reproductive and respiratory syndrome on swine production in the United States.

          To estimate the annual cost of infections attributable to porcine reproductive and respiratory syndrome (PRRS) virus to US swine producers. Economic analysis. Data on the health and productivity of PRRS-affected and PRRS-unaffected breeding herds and growing-pig populations were collected from a convenience sample of swine farms in the midwestern United States. Health and productivity variables of PRRS-affected and PRRS-unaffected swine farms were analyzed to estimate the impact of PRRS on specific farms. National estimates of PRRS incidence were then used to determine the annual economic impact of PRRS on US swine producers. PRRS affected breeding herds and growing-pig populations as measured by a decrease in reproductive health, an increase in deaths, and reductions in the rate and efficiency of growth. Total annual economic impact of these effects on US swine producers was estimated at dollar 66.75 million in breeding herds and dollar 493.57 million in growing-pig populations. PRRS imposes a substantial financial burden on US swine producers and causes approximately dollar 560.32 million in losses each year. By comparison, prior to eradication, annual losses attributable to classical swine fever (hog cholera) and pseudorabies were estimated at dollar 364.09 million and dollar 36.27 million, respectively (adjusted on the basis of year 2004 dollars). Current PRRS control strategies are not predictably successful; thus, PRRS-associated losses will continue into the future. Research to improve our understanding of ecologic and epidemiologic characteristics of the PRRS virus and technologic advances (vaccines and diagnostic tests) to prevent clinical effects are warranted.
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            Pulmonary dendritic cells producing IL-10 mediate tolerance induced by respiratory exposure to antigen.

            Respiratory exposure to allergen induces T cell tolerance and protection against the development of airway hyperreactivity and asthma. However, the specific mechanisms by which tolerance is induced by respiratory allergen are not clear. We report here that pulmonary dendritic cells (DCs) from mice exposed to respiratory antigen transiently produced interleukin 10 (IL-10). These phenotypically mature pulmonary DCs, which were B-7(hi) as well as producing IL-10, stimulated the development of CD4(+) T regulatory 1--like cells that also produced high amounts of IL-10. In addition, adoptive transfer of pulmonary DCs from IL-10(+/+), but not IL-10(-/-), mice exposed to respiratory antigen induced antigen-specific unresponsiveness in recipient mice. These studies show that IL-10 production by DCs is critical for the induction of tolerance, and that phenotypically mature pulmonary DCs mediate tolerance induced by respiratory exposure to antigen.
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              Antigen presentation in the thymus for positive selection and central tolerance induction.

              Understanding how thymic selection imparts self-peptide-MHC complex restriction and a high degree of self tolerance on the T cell repertoire requires a detailed description of the parameters that shape the MHC ligand repertoire of distinct thymic antigen-presenting cells and of how these cells communicate with T cells. Several recent discoveries pertaining to cortex-specific pathways of antigen processing, the heterogeneity of thymic dendritic cells and the intercellular transfer of self antigens have uncovered surprising and unique aspects of antigen presentation in the thymic microenvironment. Here, we discuss these new findings in the context of how individual thymic stromal cell types support T cell selection in a cooperative rather than a redundant manner.
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                Author and article information

                Contributors
                319 335-9006 , john-butler@uiowa.edu
                Kelly.lager@ars.usda.gov
                631-323-3006 , William.golde@ars-usda.gov
                515-337-7428 , Kay.faaberg@ars.usda.gov
                Marek.sinkora@tiscali.cz
                515-337-7428 , Crystal.loving@ars.usda.gov
                zhangyi@umd.edu
                Journal
                Immunol Res
                Immunol. Res
                Immunologic Research
                Springer US (New York )
                0257-277X
                1559-0755
                1 July 2014
                2014
                : 59
                : 1
                : 81-108
                Affiliations
                [1 ]GRID grid.214572.7, ISNI 0000000419368294, Department of Microbiology, Carver College of Medicine, , University of Iowa, ; Iowa City, IA USA
                [2 ]GRID grid.417548.b, ISNI 0000000404786311, Virus and Prion Research Unit, , National Animal Disease Center, ; Ames, IA USA
                [3 ]GRID grid.417548.b, ISNI 0000000404786311, Foreign Animal Disease Unit, , Plum Island Animal Disease Center, ; Greensport, NY 11944 USA
                [4 ]GRID grid.418095.1, ISNI 0000000110153316, Institute of Gnotobiology, , Czech Academy of Sciences, ; Novy Hradek, Czech Republic
                [5 ]GRID grid.411024.2, ISNI 0000000121754264, Department of Veterinary Medicine, , University of Maryland, ; 8075 Greenmead Dr. College Park, Baltimore, MD 20742 USA
                Article
                8549
                10.1007/s12026-014-8549-5
                7091131
                24981123
                61c0c5bf-63b5-4f76-b966-25daf339458b
                © Springer Science+Business Media New York 2014

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                Categories
                Immunology at the University of Iowa
                Custom metadata
                © Springer Science+Business Media New York 2014

                immune dysregulation,pandemic,economic loss,arterivirus,hypothesis

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