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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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          <name>Title</name>
          <description>A name given to the resource</description>
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              <text>Evasion by stealth: inefficient immune activation underlies poor T cell response and severe disease in SARS-CoV-infected mice.</text>
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          <name>Creator</name>
          <description>An entity primarily responsible for making the resource</description>
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              <text>Jincun Zhao, Jingxian Zhao, Nico van Rooijen, Stanley Perlman</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>Severe Acute Respiratory Syndrome caused substantial morbidity and mortality during the 2002-2003 epidemic. Many of the features of the human disease are duplicated in BALB/c mice infected with a mouse-adapted version of the virus (MA15), which develop respiratory disease with high morbidity and mortality. Here, we show that severe disease is correlated with slow kinetics of virus clearance and delayed activation and transit of respiratory dendritic cells (rDC) to the draining lymph nodes (DLN) with a consequent deficient virus-specific T cell response. All of these defects are corrected when mice are treated with liposomes containing clodronate, which deplete alveolar macrophages (AM). Inhibitory AMs are believed to prevent the development of immune responses to environmental antigens and allergic responses by interacting with lung dendritic cells and T cells. The inhibitory effects of AM can also be nullified if mice or AMs are pretreated with poly I:C, which directly activate AMs and rDCs through toll-like receptors 3 (TLR3). Further, adoptive transfer of activated but not resting bone marrow-derived dendritic cells (BMDC) protect mice from lethal MA15 infection. These results may be relevant for SARS in humans, which is also characterized by prolonged virus persistence and delayed development of a SARS-CoV-specific immune response in individuals with severe disease.</text>
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          <name>Date</name>
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              <text>2009</text>
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          <name>Identifier</name>
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              <text>DOI: 10.1371/journal.ppat.1000636</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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              <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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              <text>Biology (General), Immunologic diseases. Allergy</text>
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        </element>
        <element elementId="44">
          <name>Language</name>
          <description>A language of the resource</description>
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              <text>EN</text>
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