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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>Coronavirus gene 7 counteracts host defenses and modulates virus virulence.</text>
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          <name>Creator</name>
          <description>An entity primarily responsible for making the resource</description>
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              <text>Jazmina L. G. Cruz, Isabel Sola, Martina Bécares, Berta Alberca, Joan Plana, Luis Enjuanes, Sonia Zuñiga</text>
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          <name>Description</name>
          <description>An account of the resource</description>
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              <text>Transmissible gastroenteritis virus (TGEV) genome contains three accessory genes: 3a, 3b and 7. Gene 7 is only present in members of coronavirus genus a1, and encodes a hydrophobic protein of 78 aa. To study gene 7 function, a recombinant TGEV virus lacking gene 7 was engineered (rTGEV-Δ7). Both the mutant and the parental (rTGEV-wt) viruses showed the same growth and viral RNA accumulation kinetics in tissue cultures. Nevertheless, cells infected with rTGEV-Δ7 virus showed an increased cytopathic effect caused by an enhanced apoptosis mediated by caspase activation. Macromolecular synthesis analysis showed that rTGEV-Δ7 virus infection led to host translational shut-off and increased cellular RNA degradation compared with rTGEV-wt infection. An increase of eukaryotic translation initiation factor 2 (eIF2α) phosphorylation and an enhanced nuclease, most likely RNase L, activity were observed in rTGEV-Δ7 virus infected cells. These results suggested that the removal of gene 7 promoted an intensified dsRNA-activated host antiviral response. In protein 7 a conserved sequence motif that potentially mediates binding to protein phosphatase 1 catalytic subunit (PP1c), a key regulator of the cell antiviral defenses, was identified. We postulated that TGEV protein 7 may counteract host antiviral response by its association with PP1c. In fact, pull-down assays demonstrated the interaction between TGEV protein 7, but not a protein 7 mutant lacking PP1c binding motif, with PP1. Moreover, the interaction between protein 7 and PP1 was required, during the infection, for eIF2α dephosphorylation and inhibition of cell RNA degradation. Inoculation of newborn piglets with rTGEV-Δ7 and rTGEV-wt viruses showed that rTGEV-Δ7 virus presented accelerated growth kinetics and pathology compared with the parental virus. Overall, the results indicated that gene 7 counteracted host cell defenses, and modified TGEV persistence increasing TGEV survival. Therefore, the acquisition of gene 7 by the TGEV genome most likely has provided a selective advantage to the virus.</text>
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              <text>2011</text>
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          <name>Identifier</name>
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              <text>DOI: 10.1371/journal.ppat.1002090</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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          <name>Language</name>
          <description>A language of the resource</description>
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              <text>EN</text>
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