SrasV1, Main, Merge, bibRecord, 003D06

Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis

Identifieur interne : 003D06 ( Main/Merge ); précédent : 003D05; suivant : 003D07

Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis

Auteurs : Chia-Yen Chen [Taïwan] ; Yueh-Hsin Ping [Taïwan] ; Hsin-Chen Lee [Taïwan] ; Kuan-Hsuan Chen [Taïwan] ; Yuan-Ming Lee [Taïwan] ; Yu-Juin Chan [Taïwan] ; Te-Cheng Lien [Taïwan] ; Tjin-Shing Jap [Taïwan] ; Chi-Hung Lin [Taïwan] ; Lung-Sen Kao [Taïwan] ; Yi-Ming Arthur Chen [Taïwan]

Source :

The Journal of infectious diseases [ 0022-1899 ] ; 2007.

RBID : Pascal:07-0388620

Descripteurs français

Pascal (Inist)
- Homme, Coronavirus, Cadre lecture ouvert, Réplication, Apoptose, Mort cellulaire, Syndrome respiratoire aigu sévère.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Apoptosis, Cell death, Coronavirus, Human, Open reading frame, Replication, Severe acute respiratory syndrome.

Abstract

Background. A unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8d that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a. Methods. Western-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a. Results. Two (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis. Conclusions. ORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term>
<term>Cell death</term>
<term>Coronavirus</term>
<term>Human</term>
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<term>Replication</term>
<term>Severe acute respiratory syndrome</term>
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<term>Coronavirus</term>
<term>Cadre lecture ouvert</term>
<term>Réplication</term>
<term>Apoptose</term>
<term>Mort cellulaire</term>
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<front><div type="abstract" xml:lang="en">Background. A unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8d that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a. Methods. Western-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a. Results. Two (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis. Conclusions. ORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.</div>
</front>
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<name sortKey="Chen, Chia Yen" sort="Chen, Chia Yen" uniqKey="Chen C" first="Chia-Yen" last="Chen">Chia-Yen Chen</name>
<name sortKey="Chen, Kuan Hsuan" sort="Chen, Kuan Hsuan" uniqKey="Chen K" first="Kuan-Hsuan" last="Chen">Kuan-Hsuan Chen</name>
<name sortKey="Chen, Yi Ming Arthur" sort="Chen, Yi Ming Arthur" uniqKey="Chen Y" first="Yi-Ming Arthur" last="Chen">Yi-Ming Arthur Chen</name>
<name sortKey="Chen, Yi Ming Arthur" sort="Chen, Yi Ming Arthur" uniqKey="Chen Y" first="Yi-Ming Arthur" last="Chen">Yi-Ming Arthur Chen</name>
<name sortKey="Jap, Tjin Shing" sort="Jap, Tjin Shing" uniqKey="Jap T" first="Tjin-Shing" last="Jap">Tjin-Shing Jap</name>
<name sortKey="Kao, Lung Sen" sort="Kao, Lung Sen" uniqKey="Kao L" first="Lung-Sen" last="Kao">Lung-Sen Kao</name>
<name sortKey="Lee, Hsin Chen" sort="Lee, Hsin Chen" uniqKey="Lee H" first="Hsin-Chen" last="Lee">Hsin-Chen Lee</name>
<name sortKey="Lee, Yuan Ming" sort="Lee, Yuan Ming" uniqKey="Lee Y" first="Yuan-Ming" last="Lee">Yuan-Ming Lee</name>
<name sortKey="Lee, Yuan Ming" sort="Lee, Yuan Ming" uniqKey="Lee Y" first="Yuan-Ming" last="Lee">Yuan-Ming Lee</name>
<name sortKey="Lien, Te Cheng" sort="Lien, Te Cheng" uniqKey="Lien T" first="Te-Cheng" last="Lien">Te-Cheng Lien</name>
<name sortKey="Lin, Chi Hung" sort="Lin, Chi Hung" uniqKey="Lin C" first="Chi-Hung" last="Lin">Chi-Hung Lin</name>
<name sortKey="Ping, Yueh Hsin" sort="Ping, Yueh Hsin" uniqKey="Ping Y" first="Yueh-Hsin" last="Ping">Yueh-Hsin Ping</name>
</country>
</tree>
</affiliations>
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Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis

Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis

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