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          <element elementId="50">
            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Coronavirus</text>
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            <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>Intoxication With Endogenous Angiotensin II: A COVID-19 Hypothesis</text>
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          <name>Creator</name>
          <description>An entity primarily responsible for making the resource</description>
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              <text>Adonis Sfera, Carolina Osorio, Nyla Jafri, Eddie Lee Diaz, Jose E. Campo Maldonado</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>Severe acute respiratory syndrome coronavirus 2 has spread rapidly around the globe. However, despite its high pathogenicity and transmissibility, the severity of the associated disease, COVID-19, varies widely. While the prognosis is favorable in most patients, critical illness, manifested by respiratory distress, thromboembolism, shock, and multi-organ failure, has been reported in about 5% of cases. Several studies have associated poor COVID-19 outcomes with the exhaustion of natural killer cells and cytotoxic T cells, lymphopenia, and elevated serum levels of D-dimer. In this article, we propose a common pathophysiological denominator for these negative prognostic markers, endogenous, angiotensin II toxicity. We hypothesize that, like in avian influenza, the outlook of COVID-19 is negatively correlated with the intracellular accumulation of angiotensin II promoted by the viral blockade of its degrading enzyme receptors. In this model, upregulated angiotensin II causes premature vascular senescence, leading to dysfunctional coagulation, and immunity. We further hypothesize that angiotensin II blockers and immune checkpoint inhibitors may be salutary for COVID-19 patients with critical illness by reversing both the clotting and immune defects (Graphical Abstract).</text>
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          <name>Date</name>
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              <text>2020</text>
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          <name>Subject</name>
          <description>The topic of the resource</description>
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              <text>Prognosis, critical illness, Angiotensin II, cellular senescence, immune checkpoint inhibitors, SARS-CoV-2</text>
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          <name>Identifier</name>
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              <text>DOI: 10.3389/fimmu.2020.01472</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>Frontiers in Immunology</text>
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          <name>Publisher</name>
          <description>An entity responsible for making the resource available</description>
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              <text>Frontiers Media S.A.</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>Immunologic diseases. Allergy</text>
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