Severe acute respiratory syndrome coronavirus spike protein counteracts BST2‐mediated restriction of virus‐like particle release / (Record no. 1789)

MARC details
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fixed length control field 02280nam a22002177a 4500
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control field DOH
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control field 20201121114613.0
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Title Severe acute respiratory syndrome coronavirus spike protein counteracts BST2‐mediated restriction of virus‐like particle release /
Statement of responsibility, etc. Shiu‐Mei Wang [and two others]
520 3# - SUMMARY, ETC.
Summary, etc. 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.
580 ## - LINKING ENTRY COMPLEXITY NOTE
Linking entry complexity note In: J Med Virol. 2019 vol. 91 (10) page: 1743–1750.<br/>Published online 2019 Jul 10. doi: 10.1002/jmv.25518
650 #2 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element SARS Virus
General subdivision classification
650 #2 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element SARS Virus
General subdivision genetics
650 #2 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element SARS Virus
General subdivision metabolism
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Wang, Shiu‐Mei
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Huang, Kuo‐Jung
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Wangcorres, Chin‐Tien
856 ## - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7166632/">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7166632/</a>
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Koha item type COVID 19 Resource
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-- 1789
-- 1789
Holdings
Withdrawn status Lost status Damaged status Not for loan Home library Current library Shelving location Date acquired Total Checkouts Full call number Barcode Date last seen Price effective from Koha item type
        DOH Central Library DOH Central Library Electronic Resource Section 11/21/2020   COVID-19-000056 D0001C000056 11/21/2020 11/21/2020 COVID 19 Resource