Open Reading Frame 8a of the Human Severe Acute Respiratory Syndrome Coronavirus Not Only Promotes Viral Replication but Also Induces Apoptosis
Identifieur interne : 003963 ( Main/Merge ); précédent : 003962; suivant : 003964Open Reading Frame 8a of the Human Severe Acute Respiratory Syndrome Coronavirus Not Only Promotes Viral Replication but Also Induces Apoptosis
Auteurs : Chia-Yen Chen [République populaire de Chine] ; Yueh-Hsin Ping [République populaire de Chine] ; Hsin-Chen Lee [République populaire de Chine] ; Kuan-Hsuan Chen [République populaire de Chine] ; Yuan-Ming Lee [République populaire de Chine] ; Yu-Juin Chan [République populaire de Chine] ; Te-Cheng Lien [République populaire de Chine] ; Tjin-Shing Jap [République populaire de Chine] ; Chi-Hung Lin [République populaire de Chine] ; Lung-Sen Kao [République populaire de Chine] ; Yi-Ming Arthur Chen [République populaire de Chine, Taïwan]Source :
- The Journal of Infectious Diseases [ 0022-1899 ] ; 2007.
Descripteurs français
- KwdFr :
- Animaux, Apoptose (physiologie), Cadres ouverts de lecture, Caspase-3 (métabolisme), Consommation d'oxygène (physiologie), Espèces réactives de l'oxygène (métabolisme), Facteurs temps, Humains, Lignée cellulaire, Petit ARN interférent, Réplication virale (physiologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (génétique).
- MESH :
- génétique : Virus du SRAS.
- métabolisme : Caspase-3, Espèces réactives de l'oxygène.
- physiologie : Apoptose, Consommation d'oxygène, Réplication virale.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Cadres ouverts de lecture, Facteurs temps, Humains, Lignée cellulaire, Petit ARN interférent.
English descriptors
- KwdEn :
- Animals, Apoptosis (physiology), Caspase 3 (metabolism), Cell Line, Chlorocebus aethiops, Humans, Open Reading Frames, Oxygen Consumption (physiology), RNA, Small Interfering, Reactive Oxygen Species (metabolism), SARS Virus (genetics), Severe Acute Respiratory Syndrome (virology), Time Factors, Virus Replication (physiology).
- MESH :
- chemical , metabolism : Caspase 3, Reactive Oxygen Species.
- genetics : SARS Virus.
- physiology : Apoptosis, Oxygen Consumption, Virus Replication.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Chlorocebus aethiops, Humans, Open Reading Frames, RNA, Small Interfering, Time Factors.
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.
Url:
DOI: 10.1086/519166
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<term>Cell Line</term>
<term>Chlorocebus aethiops</term>
<term>Humans</term>
<term>Open Reading Frames</term>
<term>Oxygen Consumption (physiology)</term>
<term>RNA, Small Interfering</term>
<term>Reactive Oxygen Species (metabolism)</term>
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<term>Severe Acute Respiratory Syndrome (virology)</term>
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<term>Consommation d'oxygène (physiologie)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Facteurs temps</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Petit ARN interférent</term>
<term>Réplication virale (physiologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Virus du SRAS (génétique)</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus du SRAS</term>
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<term>Espèces réactives de l'oxygène</term>
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<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term>
<term>Consommation d'oxygène</term>
<term>Réplication virale</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term>
<term>Oxygen Consumption</term>
<term>Virus Replication</term>
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<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
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<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
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<term>Cell Line</term>
<term>Chlorocebus aethiops</term>
<term>Humans</term>
<term>Open Reading Frames</term>
<term>RNA, Small Interfering</term>
<term>Time Factors</term>
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<term>Cadres ouverts de lecture</term>
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<front><div type="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.</div>
</front>
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<author><name sortKey="Chen, Kuan Hsuan" sort="Chen, Kuan Hsuan" uniqKey="Chen K" first="Kuan-Hsuan" last="Chen">Kuan-Hsuan Chen</name>
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<wicri:regionArea>AIDS Prevention and Research Center, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Lee, Yuan Ming" sort="Lee, Yuan Ming" uniqKey="Lee Y" first="Yuan-Ming" last="Lee">Yuan-Ming Lee</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Istitute of Public Health, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Division of Clinical Virology, Department of Pathology and Laboratory Medicine, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Chan, Yu Juin" sort="Chan, Yu Juin" uniqKey="Chan Y" first="Yu-Juin" last="Chan">Yu-Juin Chan</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Division of Clinical Virology, Department of Pathology and Laboratory Medicine, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Lien, Te Cheng" sort="Lien, Te Cheng" uniqKey="Lien T" first="Te-Cheng" last="Lien">Te-Cheng Lien</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Respiratory Therapy, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Jap, Tjin Shing" sort="Jap, Tjin Shing" uniqKey="Jap T" first="Tjin-Shing" last="Jap">Tjin-Shing Jap</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Section of Biochemistry, Department of Pathology and Laboratory Medicine, Veterans General Hospital, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Lin, Chi Hung" sort="Lin, Chi Hung" uniqKey="Lin C" first="Chi-Hung" last="Lin">Chi-Hung Lin</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Institute of Microbiology and Immunology, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Kao, Lung Sen" sort="Kao, Lung Sen" uniqKey="Kao L" first="Lung-Sen" last="Kao">Lung-Sen Kao</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Faculty of Life Science, National Yang-Ming University, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
</author>
<author><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>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Istitute of Public Health, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>AIDS Prevention and Research Center, Taipei, Taiwan</wicri:regionArea>
<wicri:noRegion>Taiwan</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country wicri:rule="url">Taïwan</country>
</affiliation>
<affiliation wicri:level="1"><country wicri:rule="url">Taïwan</country>
<wicri:regionArea>Reprints or correspondence: Prof. Yi-Ming A Chen, AIDS Prevention and Research Center, National Yang-Ming University, Li-Noun Street, Section 2, Taipei</wicri:regionArea>
<wicri:noRegion>Taipei</wicri:noRegion>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j" type="main">The Journal of Infectious Diseases</title>
<title level="j" type="abbrev">The Journal of Infectious Diseases</title>
<idno type="ISSN">0022-1899</idno>
<idno type="eISSN">1537-6613</idno>
<imprint><publisher>The University of Chicago Press</publisher>
<date type="published">2007</date>
<biblScope unit="vol">196</biblScope>
<biblScope unit="issue">3</biblScope>
<biblScope unit="page" from="405">405</biblScope>
<biblScope unit="page" to="415">415</biblScope>
</imprint>
<idno type="ISSN">0022-1899</idno>
</series>
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<front><div type="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.</div>
</front>
</TEI>
</ISTEX>
<PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis.</title>
<author><name sortKey="Chen, Chia Yen" sort="Chen, Chia Yen" uniqKey="Chen C" first="Chia-Yen" last="Chen">Chia-Yen Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Institute of Public Health, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation>
<country xml:lang="fr">Taïwan</country>
<wicri:regionArea>Institute of Public Health, National Yang-Ming University, Taipei</wicri:regionArea>
<wicri:noRegion>Taipei</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Ping, Yueh Hsin" sort="Ping, Yueh Hsin" uniqKey="Ping Y" first="Yueh-Hsin" last="Ping">Yueh-Hsin Ping</name>
</author>
<author><name sortKey="Lee, Hsin Chen" sort="Lee, Hsin Chen" uniqKey="Lee H" first="Hsin-Chen" last="Lee">Hsin-Chen Lee</name>
</author>
<author><name sortKey="Chen, Kuan Hsuan" sort="Chen, Kuan Hsuan" uniqKey="Chen K" first="Kuan-Hsuan" last="Chen">Kuan-Hsuan Chen</name>
</author>
<author><name sortKey="Lee, Yuan Ming" sort="Lee, Yuan Ming" uniqKey="Lee Y" first="Yuan-Ming" last="Lee">Yuan-Ming Lee</name>
</author>
<author><name sortKey="Chan, Yu Juin" sort="Chan, Yu Juin" uniqKey="Chan Y" first="Yu-Juin" last="Chan">Yu-Juin Chan</name>
</author>
<author><name sortKey="Lien, Te Cheng" sort="Lien, Te Cheng" uniqKey="Lien T" first="Te-Cheng" last="Lien">Te-Cheng Lien</name>
</author>
<author><name sortKey="Jap, Tjin Shing" sort="Jap, Tjin Shing" uniqKey="Jap T" first="Tjin-Shing" last="Jap">Tjin-Shing Jap</name>
</author>
<author><name sortKey="Lin, Chi Hung" sort="Lin, Chi Hung" uniqKey="Lin C" first="Chi-Hung" last="Lin">Chi-Hung Lin</name>
</author>
<author><name sortKey="Kao, Lung Sen" sort="Kao, Lung Sen" uniqKey="Kao L" first="Lung-Sen" last="Kao">Lung-Sen Kao</name>
</author>
<author><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>
</author>
</titleStmt>
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<date when="2007">2007</date>
<idno type="RBID">pubmed:17597455</idno>
<idno type="pmid">17597455</idno>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis.</title>
<author><name sortKey="Chen, Chia Yen" sort="Chen, Chia Yen" uniqKey="Chen C" first="Chia-Yen" last="Chen">Chia-Yen Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Institute of Public Health, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation>
<country xml:lang="fr">Taïwan</country>
<wicri:regionArea>Institute of Public Health, National Yang-Ming University, Taipei</wicri:regionArea>
<wicri:noRegion>Taipei</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Ping, Yueh Hsin" sort="Ping, Yueh Hsin" uniqKey="Ping Y" first="Yueh-Hsin" last="Ping">Yueh-Hsin Ping</name>
</author>
<author><name sortKey="Lee, Hsin Chen" sort="Lee, Hsin Chen" uniqKey="Lee H" first="Hsin-Chen" last="Lee">Hsin-Chen Lee</name>
</author>
<author><name sortKey="Chen, Kuan Hsuan" sort="Chen, Kuan Hsuan" uniqKey="Chen K" first="Kuan-Hsuan" last="Chen">Kuan-Hsuan Chen</name>
</author>
<author><name sortKey="Lee, Yuan Ming" sort="Lee, Yuan Ming" uniqKey="Lee Y" first="Yuan-Ming" last="Lee">Yuan-Ming Lee</name>
</author>
<author><name sortKey="Chan, Yu Juin" sort="Chan, Yu Juin" uniqKey="Chan Y" first="Yu-Juin" last="Chan">Yu-Juin Chan</name>
</author>
<author><name sortKey="Lien, Te Cheng" sort="Lien, Te Cheng" uniqKey="Lien T" first="Te-Cheng" last="Lien">Te-Cheng Lien</name>
</author>
<author><name sortKey="Jap, Tjin Shing" sort="Jap, Tjin Shing" uniqKey="Jap T" first="Tjin-Shing" last="Jap">Tjin-Shing Jap</name>
</author>
<author><name sortKey="Lin, Chi Hung" sort="Lin, Chi Hung" uniqKey="Lin C" first="Chi-Hung" last="Lin">Chi-Hung Lin</name>
</author>
<author><name sortKey="Kao, Lung Sen" sort="Kao, Lung Sen" uniqKey="Kao L" first="Lung-Sen" last="Kao">Lung-Sen Kao</name>
</author>
<author><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>
</author>
</analytic>
<series><title level="j">The Journal of infectious diseases</title>
<idno type="ISSN">0022-1899</idno>
<imprint><date when="2007" type="published">2007</date>
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<term>Apoptosis (physiology)</term>
<term>Caspase 3 (metabolism)</term>
<term>Cell Line</term>
<term>Chlorocebus aethiops</term>
<term>Humans</term>
<term>Open Reading Frames</term>
<term>Oxygen Consumption (physiology)</term>
<term>RNA, Small Interfering</term>
<term>Reactive Oxygen Species (metabolism)</term>
<term>SARS Virus (genetics)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Time Factors</term>
<term>Virus Replication (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Apoptose (physiologie)</term>
<term>Cadres ouverts de lecture</term>
<term>Caspase-3 (métabolisme)</term>
<term>Consommation d'oxygène (physiologie)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Facteurs temps</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Petit ARN interférent</term>
<term>Réplication virale (physiologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Virus du SRAS (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 3</term>
<term>Reactive Oxygen Species</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term>
<term>Espèces réactives de l'oxygène</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term>
<term>Consommation d'oxygène</term>
<term>Réplication virale</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term>
<term>Oxygen Consumption</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Chlorocebus aethiops</term>
<term>Humans</term>
<term>Open Reading Frames</term>
<term>RNA, Small Interfering</term>
<term>Time Factors</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cadres ouverts de lecture</term>
<term>Facteurs temps</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Petit ARN interférent</term>
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<front><div type="abstract" xml:lang="en">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) 8a' 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.</div>
</front>
</TEI>
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