MicroRNome Analysis Unravels the Molecular Basis of SARS Infection in Bronchoalveolar Stem Cells
Identifieur interne : 000D71 ( Main/Exploration ); précédent : 000D70; suivant : 000D72MicroRNome Analysis Unravels the Molecular Basis of SARS Infection in Bronchoalveolar Stem Cells
Auteurs : Bibekanand Mallick [Inde] ; Zhumur Ghosh [États-Unis] ; Jayprokas Chakrabarti [Inde]Source :
- PLoS ONE [ 1932-6203 ] ; 2009.
Abstract
Severe acute respiratory syndrome (SARS), caused by the coronavirus SARS-CoV, is an acute infectious disease with significant mortality. A typical clinical feature associated with SARS is pulmonary fibrosis and associated lung failure. In the aftermath of the SARS epidemic, although significant progress towards understanding the underlying molecular mechanism of the infection has been made, a large gap still remains in our knowledge regarding how SARS-CoV interacts with the host cell at the onset of infection. The rapidly changing viral genome adds another variable to this equation. We have focused on a novel concept of microRNA (miRNA)–mediated host–virus interactions in bronchoalveolar stem cells (BASCs) at the onset of infection by correlating the “BASC–microRNome” with their targets within BASCs and viral genome. This work encompasses miRNA array data analysis, target prediction, and miRNA–mRNA enrichment analysis and develops a complex interaction map among disease-related factors, miRNAs, and BASCs in SARS pathway, which will provide some clues for diagnostic markers to view an overall interplay leading to disease progression. Our observation reveals the BASCs (Sca-1+ CD34+ CD45- Pecam-), a subset of Oct-4+ ACE2+ epithelial colony cells at the broncho-alveolar duct junction, to be the prime target cells of SARS-CoV infection. Upregulated BASC miRNAs-17*, -574-5p, and -214 are co-opted by SARS-CoV to suppress its own replication and evade immune elimination until successful transmission takes place. Viral Nucleocapsid and Spike protein targets seem to co-opt downregulated miR-223 and miR-98 respectively within BASCs to control the various stages of BASC differentiation, activation of inflammatory chemokines, and downregulation of ACE2. All these effectively accounts for a successful viral transmission and replication within BASCs causing continued deterioration of lung tissues and apparent loss of capacity for lung repair. Overall, this investigation reveals another mode of exploitation of cellular miRNA machinery by virus to their own advantage.
Url:
DOI: 10.1371/journal.pone.0007837
PubMed: 19915717
PubMed Central: 2773932
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">MicroRNome Analysis Unravels the Molecular Basis of SARS Infection in Bronchoalveolar Stem Cells</title><author><name sortKey="Mallick, Bibekanand" sort="Mallick, Bibekanand" uniqKey="Mallick B" first="Bibekanand" last="Mallick">Bibekanand Mallick</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Computational Biology Group, Indian Association for the Cultivation of Science, Calcutta, India</addr-line></nlm:aff><country xml:lang="fr">Inde</country><wicri:regionArea>Computational Biology Group, Indian Association for the Cultivation of Science, Calcutta</wicri:regionArea><wicri:noRegion>Calcutta</wicri:noRegion></affiliation></author><author><name sortKey="Ghosh, Zhumur" sort="Ghosh, Zhumur" uniqKey="Ghosh Z" first="Zhumur" last="Ghosh">Zhumur Ghosh</name><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Department of Medicine and Department of Radiology, Stanford University School of Medicine, Stanford, California, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine and Department of Radiology, Stanford University School of Medicine, Stanford, California</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Chakrabarti, Jayprokas" sort="Chakrabarti, Jayprokas" uniqKey="Chakrabarti J" first="Jayprokas" last="Chakrabarti">Jayprokas Chakrabarti</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Computational Biology Group, Indian Association for the Cultivation of Science, Calcutta, India</addr-line></nlm:aff><country xml:lang="fr">Inde</country><wicri:regionArea>Computational Biology Group, Indian Association for the Cultivation of Science, Calcutta</wicri:regionArea><wicri:noRegion>Calcutta</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno 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type="wicri:Area/Main/Exploration">000D71</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">MicroRNome Analysis Unravels the Molecular Basis of SARS Infection in Bronchoalveolar Stem Cells</title><author><name sortKey="Mallick, Bibekanand" sort="Mallick, Bibekanand" uniqKey="Mallick B" first="Bibekanand" last="Mallick">Bibekanand Mallick</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Computational Biology Group, Indian Association for the Cultivation of Science, Calcutta, India</addr-line></nlm:aff><country xml:lang="fr">Inde</country><wicri:regionArea>Computational Biology Group, Indian Association for the Cultivation of Science, Calcutta</wicri:regionArea><wicri:noRegion>Calcutta</wicri:noRegion></affiliation></author><author><name sortKey="Ghosh, Zhumur" sort="Ghosh, Zhumur" uniqKey="Ghosh Z" first="Zhumur" last="Ghosh">Zhumur Ghosh</name><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Department of Medicine and Department of Radiology, Stanford University School of Medicine, Stanford, California, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine and Department of Radiology, Stanford University School of Medicine, Stanford, California</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Chakrabarti, Jayprokas" sort="Chakrabarti, Jayprokas" uniqKey="Chakrabarti J" first="Jayprokas" last="Chakrabarti">Jayprokas Chakrabarti</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Computational Biology Group, Indian Association for the Cultivation of Science, Calcutta, India</addr-line></nlm:aff><country xml:lang="fr">Inde</country><wicri:regionArea>Computational Biology Group, Indian Association for the Cultivation of Science, Calcutta</wicri:regionArea><wicri:noRegion>Calcutta</wicri:noRegion></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome (SARS), caused by the coronavirus SARS-CoV, is an acute infectious disease with significant mortality. A typical clinical feature associated with SARS is pulmonary fibrosis and associated lung failure. In the aftermath of the SARS epidemic, although significant progress towards understanding the underlying molecular mechanism of the infection has been made, a large gap still remains in our knowledge regarding how SARS-CoV interacts with the host cell at the onset of infection. The rapidly changing viral genome adds another variable to this equation. We have focused on a novel concept of microRNA (miRNA)–mediated host–virus interactions in bronchoalveolar stem cells (BASCs) at the onset of infection by correlating the “BASC–microRNome” with their targets within BASCs and viral genome. This work encompasses miRNA array data analysis, target prediction, and miRNA–mRNA enrichment analysis and develops a complex interaction map among disease-related factors, miRNAs, and BASCs in SARS pathway, which will provide some clues for diagnostic markers to view an overall interplay leading to disease progression. Our observation reveals the BASCs (Sca-1+ CD34+ CD45- Pecam-), a subset of Oct-4+ ACE2+ epithelial colony cells at the broncho-alveolar duct junction, to be the prime target cells of SARS-CoV infection. Upregulated BASC miRNAs-17*, -574-5p, and -214 are co-opted by SARS-CoV to suppress its own replication and evade immune elimination until successful transmission takes place. Viral Nucleocapsid and Spike protein targets seem to co-opt downregulated miR-223 and miR-98 respectively within BASCs to control the various stages of BASC differentiation, activation of inflammatory chemokines, and downregulation of ACE2. All these effectively accounts for a successful viral transmission and replication within BASCs causing continued deterioration of lung tissues and apparent loss of capacity for lung repair. Overall, this investigation reveals another mode of exploitation of cellular miRNA machinery by virus to their own advantage.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Donnelly, Ca" uniqKey="Donnelly C">CA Donnelly</name></author><author><name sortKey="Ghani, Ac" uniqKey="Ghani A">AC Ghani</name></author><author><name sortKey="Leung, Gm" uniqKey="Leung G">GM Leung</name></author><author><name sortKey="Hedley, Aj" uniqKey="Hedley A">AJ Hedley</name></author><author><name sortKey="Fraser, C" uniqKey="Fraser C">C Fraser</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ksiazek, Tg" uniqKey="Ksiazek T">TG Ksiazek</name></author><author><name sortKey="Erdman, D" uniqKey="Erdman D">D Erdman</name></author><author><name sortKey="Goldsmith, Cs" uniqKey="Goldsmith C">CS Goldsmith</name></author><author><name sortKey="Zaki, Sr" uniqKey="Zaki S">SR Zaki</name></author><author><name sortKey="Peret, T" 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sortKey="Farh, Kk" uniqKey="Farh K">KK Farh</name></author><author><name sortKey="Johnston, Wk" uniqKey="Johnston W">WK Johnston</name></author><author><name sortKey="Garrett Engele, P" uniqKey="Garrett Engele P">P Garrett-Engele</name></author><author><name sortKey="Lim, Lp" uniqKey="Lim L">LP Lim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Friedman, Rc" uniqKey="Friedman R">RC Friedman</name></author><author><name sortKey="Farh, Kk" uniqKey="Farh K">KK Farh</name></author><author><name sortKey="Burge, Cb" uniqKey="Burge C">CB Burge</name></author><author><name sortKey="Bartel, Dp" uniqKey="Bartel D">DP Bartel</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bartel, Dp" uniqKey="Bartel D">DP Bartel</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bolstad, Bm" uniqKey="Bolstad B">BM Bolstad</name></author><author><name sortKey="Irizarry, Ra" uniqKey="Irizarry R">RA Irizarry</name></author><author><name sortKey="Astrand, M" uniqKey="Astrand M">M Astrand</name></author><author><name sortKey="Speed, Tp" uniqKey="Speed T">TP Speed</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Inde</li><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="Inde"><noRegion><name sortKey="Mallick, Bibekanand" sort="Mallick, Bibekanand" uniqKey="Mallick B" first="Bibekanand" last="Mallick">Bibekanand Mallick</name></noRegion><name sortKey="Chakrabarti, Jayprokas" sort="Chakrabarti, Jayprokas" uniqKey="Chakrabarti J" first="Jayprokas" last="Chakrabarti">Jayprokas Chakrabarti</name></country><country name="États-Unis"><region name="Californie"><name sortKey="Ghosh, Zhumur" sort="Ghosh, Zhumur" uniqKey="Ghosh Z" first="Zhumur" last="Ghosh">Zhumur Ghosh</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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