Severe acute respiratory syndrome coronavirus spike protein counteracts BST2-mediated restriction of virus-like particle release.
Identifieur interne : 000A92 ( Main/Exploration ); précédent : 000A91; suivant : 000A93Severe acute respiratory syndrome coronavirus spike protein counteracts BST2-mediated restriction of virus-like particle release.
Auteurs : Shiu-Mei Wang [Taïwan] ; Kuo-Jung Huang [Taïwan] ; Chin-Tien Wang [Taïwan]Source :
- Journal of medical virology [ 1096-9071 ] ; 2019.
Abstract
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.
DOI: 10.1002/jmv.25518
PubMed: 31199522
Affiliations:
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Huang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Research, Taipei Veterans General Hospital and Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Research, Taipei Veterans General Hospital and Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Chin Tien" sort="Wang, Chin Tien" uniqKey="Wang C" first="Chin-Tien" last="Wang">Chin-Tien Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Research, Taipei Veterans General Hospital and Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Research, Taipei 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Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Huang, Kuo Jung" sort="Huang, Kuo Jung" uniqKey="Huang K" first="Kuo-Jung" last="Huang">Kuo-Jung Huang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Research, Taipei Veterans General Hospital and Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Research, Taipei Veterans General Hospital and Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Chin Tien" sort="Wang, Chin Tien" uniqKey="Wang C" first="Chin-Tien" last="Wang">Chin-Tien Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Research, Taipei Veterans General Hospital and Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Research, Taipei Veterans General Hospital and Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of medical virology</title><idno type="eISSN">1096-9071</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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 glycosylation<sup>1</sup> . 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.</div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Wang, Shiu Mei" sort="Wang, Shiu Mei" uniqKey="Wang S" first="Shiu-Mei" last="Wang">Shiu-Mei Wang</name></noRegion><name sortKey="Huang, Kuo Jung" sort="Huang, Kuo Jung" uniqKey="Huang K" first="Kuo-Jung" last="Huang">Kuo-Jung Huang</name><name sortKey="Wang, Chin Tien" sort="Wang, Chin Tien" uniqKey="Wang C" first="Chin-Tien" last="Wang">Chin-Tien Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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