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The human severe acute respiratory syndrome coronavirus (SARS-CoV) 8b protein is distinct from its counterpart in animal SARS-CoV and down-regulates the expression of the envelope protein in infected cells

Identifieur interne : 001031 ( Pmc/Checkpoint ); précédent : 001030; suivant : 001032

The human severe acute respiratory syndrome coronavirus (SARS-CoV) 8b protein is distinct from its counterpart in animal SARS-CoV and down-regulates the expression of the envelope protein in infected cells

Auteurs : Choong-Tat Keng ; Yook-Wah Choi ; Matthijs R. A. Welkers ; Daphne Z. L. Chan ; Shuo Shen ; Seng Gee Lim ; Wanjin Hong ; Yee-Joo Tan

Source :

RBID : PMC:7111915

Abstract

The severe acute respiratory syndrome coronavirus (SARS-CoV), isolated from humans infected during the peak of epidemic, encodes two accessory proteins termed as 8a and 8b. Interestingly, the SARS-CoV isolated from animals contains an extra 29-nucleotide in this region such that these proteins are fused to become a single protein, 8ab. Here, we compared the cellular properties of the 8a, 8b and 8ab proteins by examining their cellular localizations and their abilities to interact with other SARS-CoV proteins. These results may suggest that the conformations of 8a and 8b are different from 8ab although nearly all the amino acids in 8a and 8b are found in 8ab. In addition, the expression of the structural protein, envelope (E), was down-regulated by 8b but not 8a or 8ab. Consequently, E was not detectable in SARS-CoV-infected cells that were expressing high levels of 8b. These findings suggest that 8b may modulate viral replication and/or pathogenesis.


Url:
DOI: 10.1016/j.virol.2006.06.026
PubMed: 16876844
PubMed Central: 7111915


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PMC:7111915

Le document en format XML

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<p>The severe acute respiratory syndrome coronavirus (SARS-CoV), isolated from humans infected during the peak of epidemic, encodes two accessory proteins termed as 8a and 8b. Interestingly, the SARS-CoV isolated from animals contains an extra 29-nucleotide in this region such that these proteins are fused to become a single protein, 8ab. Here, we compared the cellular properties of the 8a, 8b and 8ab proteins by examining their cellular localizations and their abilities to interact with other SARS-CoV proteins. These results may suggest that the conformations of 8a and 8b are different from 8ab although nearly all the amino acids in 8a and 8b are found in 8ab. In addition, the expression of the structural protein, envelope (E), was down-regulated by 8b but not 8a or 8ab. Consequently, E was not detectable in SARS-CoV-infected cells that were expressing high levels of 8b. These findings suggest that 8b may modulate viral replication and/or pathogenesis.</p>
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</TEI>
<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Virology</journal-id>
<journal-id journal-id-type="iso-abbrev">Virology</journal-id>
<journal-title-group>
<journal-title>Virology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0042-6822</issn>
<issn pub-type="epub">1096-0341</issn>
<publisher>
<publisher-name>Elsevier Inc.</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">16876844</article-id>
<article-id pub-id-type="pmc">7111915</article-id>
<article-id pub-id-type="publisher-id">S0042-6822(06)00415-6</article-id>
<article-id pub-id-type="doi">10.1016/j.virol.2006.06.026</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>The human severe acute respiratory syndrome coronavirus (SARS-CoV) 8b protein is distinct from its counterpart in animal SARS-CoV and down-regulates the expression of the envelope protein in infected cells</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Keng</surname>
<given-names>Choong-Tat</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Choi</surname>
<given-names>Yook-Wah</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Welkers</surname>
<given-names>Matthijs R.A.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Chan</surname>
<given-names>Daphne Z.L.</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Shen</surname>
<given-names>Shuo</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Gee Lim</surname>
<given-names>Seng</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Hong</surname>
<given-names>Wanjin</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Tan</surname>
<given-names>Yee-Joo</given-names>
</name>
<email>mcbtanyj@imcb.a-star.edu.sg</email>
<xref rid="cor1" ref-type="corresp"></xref>
</contrib>
</contrib-group>
<aff>Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore, 138673</aff>
<author-notes>
<corresp id="cor1">
<label></label>
Corresponding author. Fax: +65 67791117.
<email>mcbtanyj@imcb.a-star.edu.sg</email>
</corresp>
</author-notes>
<pub-date pub-type="pmc-release">
<day>31</day>
<month>7</month>
<year>2006</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub">
<day>10</day>
<month>10</month>
<year>2006</year>
</pub-date>
<pub-date pub-type="epub">
<day>31</day>
<month>7</month>
<year>2006</year>
</pub-date>
<volume>354</volume>
<issue>1</issue>
<fpage>132</fpage>
<lpage>142</lpage>
<history>
<date date-type="received">
<day>10</day>
<month>4</month>
<year>2006</year>
</date>
<date date-type="rev-recd">
<day>15</day>
<month>6</month>
<year>2006</year>
</date>
<date date-type="accepted">
<day>17</day>
<month>6</month>
<year>2006</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright © 2006 Elsevier Inc. All rights reserved.</copyright-statement>
<copyright-year>2006</copyright-year>
<copyright-holder>Elsevier Inc.</copyright-holder>
<license>
<license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p>
</license>
</permissions>
<abstract>
<p>The severe acute respiratory syndrome coronavirus (SARS-CoV), isolated from humans infected during the peak of epidemic, encodes two accessory proteins termed as 8a and 8b. Interestingly, the SARS-CoV isolated from animals contains an extra 29-nucleotide in this region such that these proteins are fused to become a single protein, 8ab. Here, we compared the cellular properties of the 8a, 8b and 8ab proteins by examining their cellular localizations and their abilities to interact with other SARS-CoV proteins. These results may suggest that the conformations of 8a and 8b are different from 8ab although nearly all the amino acids in 8a and 8b are found in 8ab. In addition, the expression of the structural protein, envelope (E), was down-regulated by 8b but not 8a or 8ab. Consequently, E was not detectable in SARS-CoV-infected cells that were expressing high levels of 8b. These findings suggest that 8b may modulate viral replication and/or pathogenesis.</p>
</abstract>
<kwd-group>
<title>Keywords</title>
<kwd>Severe acute respiratory syndrome (SARS)</kwd>
<kwd>Coronavirus (CoV)</kwd>
<kwd>Accessory proteins</kwd>
<kwd>Envelope (E) protein</kwd>
<kwd>8a</kwd>
<kwd>8b</kwd>
<kwd>8ab</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations>
<list></list>
<tree>
<noCountry>
<name sortKey="Chan, Daphne Z L" sort="Chan, Daphne Z L" uniqKey="Chan D" first="Daphne Z. L." last="Chan">Daphne Z. L. Chan</name>
<name sortKey="Choi, Yook Wah" sort="Choi, Yook Wah" uniqKey="Choi Y" first="Yook-Wah" last="Choi">Yook-Wah Choi</name>
<name sortKey="Gee Lim, Seng" sort="Gee Lim, Seng" uniqKey="Gee Lim S" first="Seng" last="Gee Lim">Seng Gee Lim</name>
<name sortKey="Hong, Wanjin" sort="Hong, Wanjin" uniqKey="Hong W" first="Wanjin" last="Hong">Wanjin Hong</name>
<name sortKey="Keng, Choong Tat" sort="Keng, Choong Tat" uniqKey="Keng C" first="Choong-Tat" last="Keng">Choong-Tat Keng</name>
<name sortKey="Shen, Shuo" sort="Shen, Shuo" uniqKey="Shen S" first="Shuo" last="Shen">Shuo Shen</name>
<name sortKey="Tan, Yee Joo" sort="Tan, Yee Joo" uniqKey="Tan Y" first="Yee-Joo" last="Tan">Yee-Joo Tan</name>
<name sortKey="Welkers, Matthijs R A" sort="Welkers, Matthijs R A" uniqKey="Welkers M" first="Matthijs R. A." last="Welkers">Matthijs R. A. Welkers</name>
</noCountry>
</tree>
</affiliations>
</record>

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