MicroRNome Analysis Unravels the Molecular Basis of SARS Infection in Bronchoalveolar Stem Cells
Identifieur interne : 002A72 ( Main/Exploration ); précédent : 002A71; suivant : 002A73MicroRNome 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.
Descripteurs français
- KwdFr :
- Alvéoles pulmonaires (cytologie), Analyse de profil d'expression de gènes, Animaux, Bronches (cytologie), Cellules souches (métabolisme), Facteur de transcription Oct-3 (métabolisme), Génome viral, Humains, Nucléocapside (), Poumon (cytologie), Régulation de l'expression des gènes, Souris, Syndrome respiratoire aigu sévère (métabolisme), Virus du SRAS (métabolisme), microARN (métabolisme).
- MESH :
- cytologie : Alvéoles pulmonaires, Bronches, Poumon.
- métabolisme : Cellules souches, Facteur de transcription Oct-3, Syndrome respiratoire aigu sévère, Virus du SRAS, microARN.
- Analyse de profil d'expression de gènes, Animaux, Génome viral, Humains, Nucléocapside, Régulation de l'expression des gènes, Souris.
English descriptors
- KwdEn :
- Animals, Bronchi (cytology), Gene Expression Profiling, Gene Expression Regulation, Genome, Viral, Humans, Lung (cytology), Mice, MicroRNAs (metabolism), Nucleocapsid (chemistry), Octamer Transcription Factor-3 (metabolism), Pulmonary Alveoli (cytology), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (metabolism), Stem Cells (metabolism).
- MESH :
- chemical , metabolism : MicroRNAs, Octamer Transcription Factor-3.
- chemistry : Nucleocapsid.
- cytology : Bronchi, Lung, Pulmonary Alveoli.
- metabolism : SARS Virus, Severe Acute Respiratory Syndrome, Stem Cells.
- Animals, Gene Expression Profiling, Gene Expression Regulation, Genome, Viral, Humans, Mice.
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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Le document en format XML
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<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation</term>
<term>Genome, Viral</term>
<term>Humans</term>
<term>Lung (cytology)</term>
<term>Mice</term>
<term>MicroRNAs (metabolism)</term>
<term>Nucleocapsid (chemistry)</term>
<term>Octamer Transcription Factor-3 (metabolism)</term>
<term>Pulmonary Alveoli (cytology)</term>
<term>SARS Virus (metabolism)</term>
<term>Severe Acute Respiratory Syndrome (metabolism)</term>
<term>Stem Cells (metabolism)</term>
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<term>Analyse de profil d'expression de gènes</term>
<term>Animaux</term>
<term>Bronches (cytologie)</term>
<term>Cellules souches (métabolisme)</term>
<term>Facteur de transcription Oct-3 (métabolisme)</term>
<term>Génome viral</term>
<term>Humains</term>
<term>Nucléocapside ()</term>
<term>Poumon (cytologie)</term>
<term>Régulation de l'expression des gènes</term>
<term>Souris</term>
<term>Syndrome respiratoire aigu sévère (métabolisme)</term>
<term>Virus du SRAS (métabolisme)</term>
<term>microARN (métabolisme)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>MicroRNAs</term>
<term>Octamer Transcription Factor-3</term>
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<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Nucleocapsid</term>
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<term>Poumon</term>
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<term>Pulmonary Alveoli</term>
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<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>
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</tree>
</affiliations>
</record>
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