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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>Text</name>
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          <name>Title</name>
          <description>A name given to the resource</description>
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              <text>Pathobiological and Genomic Characterization of a Cold-Adapted Infectious Bronchitis Virus (BP-caKII)</text>
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          <name>Creator</name>
          <description>An entity primarily responsible for making the resource</description>
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              <text>Seung Min Hong, Se-Hee An, Chung-Young Lee, Chang-Seon Song, Kang-Seuk Choi, Jae-Hong Kim, Hyuk-Joon Kwon</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>We established a cold-adapted infectious bronchitis virus (BP-caKII) by passaging a field virus through specific pathogen-free embryonated eggs 20 times at 32 &amp;#176;C. We characterized its growth kinetics and pathogenicity in embryonated eggs, and its tropism and persistence in different tissues from chickens; then, we evaluated pathogenicity by using a new premature reproductive tract pathogenicity model. Furthermore, we determined the complete genomic sequence of BP-caKII to understand the genetic changes related to cold adaptation. According to our results, BP-caKII clustered with the KII genotype viruses K2 and KM91, and showed less pathogenicity than K2, a live attenuated vaccine strain. BP-caKII showed delayed viremia, resulting in its delayed dissemination to the kidneys and cecal tonsils compared to K2 and KM91, the latter of which is a pathogenic field strain. A comparative genomics study revealed similar nucleotide sequences between BP-caKII, K2 and KM91 but clearly showed different mutations among them. BP-caKII shared several mutations with K2 (nsp13, 14, 15 and 16) following embryo adaptation but acquired multiple additional mutations in nonstructural proteins (nsp3, 4 and 12), spike proteins and nucleocapsid proteins following cold adaptation. Thus, the establishment of BP-caKII and the identified mutations in this study may provide insight into the genetic background of embryo and cold adaptations, and the attenuation of coronaviruses.</text>
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          <name>Date</name>
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              <text>2018</text>
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          <name>Subject</name>
          <description>The topic of the resource</description>
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              <text>infectious bronchitis virus, Cold adaptation, Comparative genomics, premature reproductive tract pathogenicity model, Persistent infection</text>
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          <name>Identifier</name>
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              <text>DOI: 10.3390/v10110652</text>
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        <element elementId="48">
          <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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          </elementTextContainer>
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        <element elementId="45">
          <name>Publisher</name>
          <description>An entity responsible for making the resource available</description>
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            <elementText elementTextId="8438">
              <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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            <elementText elementTextId="8439">
              <text>Microbiology</text>
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          <name>Language</name>
          <description>A language of the resource</description>
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            <elementText elementTextId="8440">
              <text>EN</text>
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