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            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Coronavirus</text>
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            <name>Description</name>
            <description>An account of the resource</description>
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                <text>Dominio científico: Coronavirus</text>
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      <description>The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.</description>
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          <name>Title</name>
          <description>A name given to the resource</description>
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              <text>Exacerbated innate host response to SARS-CoV in aged non-human primates.</text>
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          <name>Creator</name>
          <description>An entity primarily responsible for making the resource</description>
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              <text>Albert D.M.E. Osterhaus, Bart L. Haagmans, Saskia L. Smits, Geert van Amerongen, Thijs Kuiken, Judith M.A. van den Brand, Marinus J. C. Eijkemans, Arno C. Andeweg, Wilfred F. van IJcken, Anna de Lang, Lonneke M Leijten</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>The emergence of viral respiratory pathogens with pandemic potential, such as severe acute respiratory syndrome coronavirus (SARS-CoV) and influenza A H5N1, urges the need for deciphering their pathogenesis to develop new intervention strategies. SARS-CoV infection causes acute lung injury (ALI) that may develop into life-threatening acute respiratory distress syndrome (ARDS) with advanced age correlating positively with adverse disease outcome. The molecular pathways, however, that cause virus-induced ALI/ARDS in aged individuals are ill-defined. Here, we show that SARS-CoV-infected aged macaques develop more severe pathology than young adult animals, even though viral replication levels are similar. Comprehensive genomic analyses indicate that aged macaques have a stronger host response to virus infection than young adult macaques, with an increase in differential expression of genes associated with inflammation, with NF-kappaB as central player, whereas expression of type I interferon (IFN)-beta is reduced. Therapeutic treatment of SARS-CoV-infected aged macaques with type I IFN reduces pathology and diminishes pro-inflammatory gene expression, including interleukin-8 (IL-8) levels, without affecting virus replication in the lungs. Thus, ALI in SARS-CoV-infected aged macaques developed as a result of an exacerbated innate host response. The anti-inflammatory action of type I IFN reveals a potential intervention strategy for virus-induced ALI.</text>
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          <name>Date</name>
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              <text>2010</text>
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          <name>Identifier</name>
          <description>An unambiguous reference to the resource within a given context</description>
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              <text>DOI: 10.1371/journal.ppat.1000756</text>
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          <name>Source</name>
          <description>A related resource from which the described resource is derived</description>
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              <text>PLoS Pathogens</text>
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          <name>Publisher</name>
          <description>An entity responsible for making the resource available</description>
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            <elementText elementTextId="27659">
              <text>Public Library of Science (PLoS)</text>
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          <name>Coverage</name>
          <description>The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant</description>
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            <elementText elementTextId="27660">
              <text>Biology (General), Immunologic diseases. Allergy</text>
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