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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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            <description>An account of the resource</description>
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                <text>Dominio científico: Coronavirus</text>
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    <description>A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.</description>
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          <name>Title</name>
          <description>A name given to the resource</description>
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              <text>Molecular Mechanism of Evolution and Human Infection with SARS-CoV-2</text>
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          <name>Creator</name>
          <description>An entity primarily responsible for making the resource</description>
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              <text>Jiahua He, Huanyu Tao, Yumeng Yan, Sheng-You Huang, Yi Xiao</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>The outbreak of a novel coronavirus, which was later formally named the severe acute respiratory coronavirus 2 (SARS-CoV-2), has caused a worldwide public health crisis. Previous studies showed that SARS-CoV-2 is highly homologous to SARS-CoV and infects humans through the binding of the spike protein to ACE2. Here, we have systematically studied the molecular mechanisms of human infection with SARS-CoV-2 and SARS-CoV by protein-protein docking and MD simulations. It was found that SARS-CoV-2 binds ACE2 with a higher affinity than SARS-CoV, which may partly explain that SARS-CoV-2 is much more infectious than SARS-CoV. In addition, the spike protein of SARS-CoV-2 has a significantly lower free energy than that of SARS-CoV, suggesting that SARS-CoV-2 is more stable and may survive a higher temperature than SARS-CoV. This provides insights into the evolution of SARS-CoV-2 because SARS-like coronaviruses have originated in bats. Our computation also suggested that the RBD-ACE2 binding for SARS-CoV-2 is much more temperature-sensitive than that for SARS-CoV. Thus, it is expected that SARS-CoV-2 would decrease its infection ability much faster than SARS-CoV when the temperature rises. These findings would be beneficial for the disease prevention and drug/vaccine development of SARS-CoV-2.</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>coronaviruses, SARS-CoV-2, SARS-CoV, human infection, molecular mechanism, protein docking</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: 10.3390/v12040428</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>Viruses</text>
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          <name>Publisher</name>
          <description>An entity responsible for making the resource available</description>
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              <text>MDPI AG</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>Microbiology</text>
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          <name>Language</name>
          <description>A language of the resource</description>
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              <text>EN</text>
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