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  <controlfield tag="001">D0001C000056</controlfield>
  <controlfield tag="003">DOH</controlfield>
  <controlfield tag="005">20201121114613.0</controlfield>
  <controlfield tag="008">201121b           ||||| |||| 00| 0 eng d</controlfield>
  <datafield tag="245" ind1="0" ind2="0">
    <subfield code="a">Severe acute respiratory syndrome coronavirus spike protein counteracts BST2&#x2010;mediated restriction of virus&#x2010;like particle release /</subfield>
    <subfield code="c">Shiu&#x2010;Mei Wang [and two others]</subfield>
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    <subfield code="a">BST2/tetherin, an interferon-inducible antiviral factor, can block the cellular release of various enveloped viruses. We previously reported that human coronavirus 229E (HCoV-229E) infection can alleviate the BST2 tethering of HIV-1 virions by downregulating cell surface BST2, suggesting that coronaviruses are capable of encoding anti-BST2 factors. Here we report our new finding that severe acute respiratory syndrome coronavirus (SARS-CoV) spike (S) glycoprotein, similar to Vpu, is capable of antagonizing the BST2 tethering of SARS-CoV, HCoV-229E, and HIV-1 virus-like particles via BST2 downregulation. However, unlike Vpu (which downmodulates BST2 by means of proteasomal and lysosomal degradation pathways), BST2 downregulation is apparently mediated by SARS-CoV S through the lysosomal degradation pathway only. We found that SARS-CoV S colocalized with both BST2 and reduced cell surface BST2, suggesting an association between SARS-CoV S and BST2 that targets the lysosomal degradation pathway. According to one recent report, SARS-CoV ORF7a antagonizes BST2 by interfering with BST2 glycosylation1 . Our data provide support for the proposal that SARS-CoV and other enveloped viruses are capable of evolving supplementary anti-BST2 factors in a manner that requires virus replication. Further experiments are required to determine whether the BST2-mediated restriction of authentic SARS-CoV virions is alleviated by the SARS-CoV spike protein.</subfield>
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    <subfield code="a">In: J Med Virol. 2019 vol.  91 (10) page: 1743&#x2013;1750.
Published online 2019 Jul 10. doi: 10.1002/jmv.25518</subfield>
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    <subfield code="a"> SARS Virus</subfield>
    <subfield code="x">classification</subfield>
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    <subfield code="a">SARS Virus</subfield>
    <subfield code="x">genetics</subfield>
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    <subfield code="a">SARS Virus</subfield>
    <subfield code="x">metabolism</subfield>
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    <subfield code="a">Wang, Shiu&#x2010;Mei </subfield>
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    <subfield code="a">Huang,  Kuo&#x2010;Jung </subfield>
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    <subfield code="a">Wangcorres,  Chin&#x2010;Tien </subfield>
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    <subfield code="u">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7166632/</subfield>
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    <subfield code="c">CV</subfield>
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    <subfield code="c">1789</subfield>
    <subfield code="d">1789</subfield>
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    <subfield code="0">0</subfield>
    <subfield code="1">0</subfield>
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    <subfield code="7">0</subfield>
    <subfield code="a">DOHCL</subfield>
    <subfield code="b">DOHCL</subfield>
    <subfield code="c">ElectronicRes</subfield>
    <subfield code="d">2020-11-21</subfield>
    <subfield code="l">0</subfield>
    <subfield code="o">COVID-19-000056</subfield>
    <subfield code="p">D0001C000056</subfield>
    <subfield code="r">2020-11-21 00:00:00</subfield>
    <subfield code="w">2020-11-21</subfield>
    <subfield code="y">CV</subfield>
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