SrasV1, Hal, Curation, bibRecord, 000133

SARS coronavirus 8b reduces viral replication by down-regulating E via an ubiquitin-independent proteasome pathway.

Identifieur interne : 000133 ( Hal/Curation ); précédent : 000132; suivant : 000134

SARS coronavirus 8b reduces viral replication by down-regulating E via an ubiquitin-independent proteasome pathway.

Auteurs : Choong-Tat Keng [Singapour] ; Sara Akerström [Suède] ; Cynthia Sau-Wai Leung [République populaire de Chine] ; Leo L M. Poon [République populaire de Chine] ; J S Malik Peiris [République populaire de Chine] ; Ali Mirazimi [Suède] ; Yee-Joo Tan [Singapour]

Source :

Microbes and Infection [ 1286-4579 ] ; 2011-02.

RBID : Hal:pasteur-00588905

Abstract

The severe acute respiratory syndrome coronavirus (SARS-CoV) 8b protein, which is not expressed by other known coronaviruses, can down-regulate the envelope (E) protein via a proteasome-dependent pathway. Here, we showed that the down-regulation of E is not dependent on the lysine residues on 8b and the reduction of polyubiquitination of E mutants is not correlated with their down-regulation by 8b, suggesting an ubiquitin-independent proteasome pathway is involved. A time-course study revealed that 8b was expressed at late-stages of SARS-CoV infection. By using Vero E6 cells stably expressing green fluorescence protein-tagged 8b, ectopic expression of 8b was shown to significantly reduce the production of progeny virus and down-regulate E expression. Taken together, these results suggest that 8b negatively modulates virus replication by down-regulating E via an ubiquitin-independent proteasome pathway.

Url:

https://hal-riip.archives-ouvertes.fr/pasteur-00588905

DOI: 10.1016/j.micinf.2010.10.017

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Le document en format XML

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<front><div type="abstract" xml:lang="en">              <p>The severe acute respiratory syndrome coronavirus (SARS-CoV) 8b protein, which is not expressed by other known coronaviruses, can down-regulate the envelope (E) protein via a proteasome-dependent pathway. Here, we showed that the down-regulation of E is not dependent on the lysine residues on 8b and the reduction of polyubiquitination of E mutants is not correlated with their down-regulation by 8b, suggesting an ubiquitin-independent proteasome pathway is involved. A time-course study revealed that 8b was expressed at late-stages of SARS-CoV infection. By using Vero E6 cells stably expressing green fluorescence protein-tagged 8b, ectopic expression of 8b was shown to significantly reduce the production of progeny virus and down-regulate E expression. Taken together, these results suggest that 8b negatively modulates virus replication by down-regulating E via an ubiquitin-independent proteasome pathway.</p>
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                <author role="aut">                  <persName>                    <forename type="first">Cynthia Sau-Wai</forename>
                    <surname>Leung</surname>
                  </persName>
                  <idno type="halauthorid">603524</idno>
                  <affiliation ref="#struct-136023"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Leo L M</forename>
                    <surname>Poon</surname>
                  </persName>
                  <idno type="halauthorid">603525</idno>
                  <affiliation ref="#struct-136023"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">J S Malik</forename>
                    <surname>Peiris</surname>
                  </persName>
                  <idno type="halauthorid">202086</idno>
                  <affiliation ref="#struct-136023"></affiliation>
                  <affiliation ref="#struct-55925"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Ali</forename>
                    <surname>Mirazimi</surname>
                  </persName>
                  <idno type="halauthorid">603526</idno>
                  <affiliation ref="#struct-156808"></affiliation>
                  <affiliation ref="#struct-99247"></affiliation>
                </author>
                <author role="crp">                  <persName>                    <forename type="first">Yee-Joo</forename>
                    <surname>Tan</surname>
                  </persName>
                  <email type="md5">70a6307807f2fb159350ecaa9aeee39d</email>
                  <email type="domain">imcb.a-star.edu.sg</email>
                  <idno type="halauthorid">603527</idno>
                  <affiliation ref="#struct-156807"></affiliation>
                  <affiliation ref="#struct-156809"></affiliation>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">17071</idno>
                <idno type="issn">1286-4579</idno>
                <title level="j">Microbes and Infection</title>
                <imprint>                  <publisher>Elsevier</publisher>
                  <biblScope unit="volume">13</biblScope>
                  <biblScope unit="issue">2</biblScope>
                  <biblScope unit="pp">179-88</biblScope>
                  <date type="datePub">2011-02</date>
                  <date type="dateEpub">2010-10-28</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1016/j.micinf.2010.10.017</idno>
              <idno type="pubmed">21035562</idno>
            </biblStruct>
          </sourceDesc>
          <profileDesc>            <langUsage>              <language ident="en">English</language>
            </langUsage>
            <textClass>              <classCode scheme="mesh">Animals</classCode>
              <classCode scheme="mesh">Cercopithecus aethiops</classCode>
              <classCode scheme="mesh">SARS Virus</classCode>
              <classCode scheme="mesh">Ubiquitin</classCode>
              <classCode scheme="mesh">Ubiquitination</classCode>
              <classCode scheme="mesh">Vero Cells</classCode>
              <classCode scheme="mesh">Viral Envelope Proteins</classCode>
              <classCode scheme="mesh">Viral Proteins</classCode>
              <classCode scheme="mesh">Virus Replication</classCode>
              <classCode scheme="mesh">Coronavirus Infections</classCode>
              <classCode scheme="mesh">Down-Regulation</classCode>
              <classCode scheme="mesh">Gene Expression Regulation, Viral</classCode>
              <classCode scheme="mesh">Gene Knockout Techniques</classCode>
              <classCode scheme="mesh">Green Fluorescent Proteins</classCode>
              <classCode scheme="mesh">Mutagenesis, Site-Directed</classCode>
              <classCode scheme="mesh">Proteasome Endopeptidase Complex</classCode>
              <classCode scheme="mesh">Protein Stability</classCode>
              <classCode scheme="halDomain" n="sdv.mp.vir">Life Sciences [q-bio]/Microbiology and Parasitology/Virology</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
            </textClass>
            <abstract xml:lang="en">              <p>The severe acute respiratory syndrome coronavirus (SARS-CoV) 8b protein, which is not expressed by other known coronaviruses, can down-regulate the envelope (E) protein via a proteasome-dependent pathway. Here, we showed that the down-regulation of E is not dependent on the lysine residues on 8b and the reduction of polyubiquitination of E mutants is not correlated with their down-regulation by 8b, suggesting an ubiquitin-independent proteasome pathway is involved. A time-course study revealed that 8b was expressed at late-stages of SARS-CoV infection. By using Vero E6 cells stably expressing green fluorescence protein-tagged 8b, ectopic expression of 8b was shown to significantly reduce the production of progeny virus and down-regulate E expression. Taken together, these results suggest that 8b negatively modulates virus replication by down-regulating E via an ubiquitin-independent proteasome pathway.</p>
            </abstract>
          </profileDesc>
        </hal>
</record>

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SARS coronavirus 8b reduces viral replication by down-regulating E via an ubiquitin-independent proteasome pathway.

SARS coronavirus 8b reduces viral replication by down-regulating E via an ubiquitin-independent proteasome pathway.

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