Cell host response to infection with novel human coronavirus EMC predicts potential antivirals and important differences with SARS coronavirus.
Identifieur interne : 001977 ( Main/Exploration ); précédent : 001976; suivant : 001978Cell host response to infection with novel human coronavirus EMC predicts potential antivirals and important differences with SARS coronavirus.
Auteurs : Laurence Josset [États-Unis] ; Vineet D. Menachery ; Lisa E. Gralinski ; Sudhakar Agnihothram ; Pavel Sova ; Victoria S. Carter ; Boyd L. Yount ; Rachel L. Graham ; Ralph S. Baric ; Michael G. KatzeSource :
- mBio [ 2150-7511 ] ; 2013.
Descripteurs français
- KwdFr :
- Cellules épithéliales (immunologie), Cellules épithéliales (virologie), Coronavirus (isolement et purification), Coronavirus (pathogénicité), Coronavirus (physiologie), Humains, Interactions hôte-pathogène, Lignée cellulaire, Réplication virale, Syndrome respiratoire aigu sévère (virologie), Tolérance immunitaire, Transcriptome.
- MESH :
- immunologie : Cellules épithéliales.
- isolement et purification : Coronavirus.
- pathogénicité : Coronavirus.
- physiologie : Coronavirus.
- virologie : Cellules épithéliales, Syndrome respiratoire aigu sévère.
- Humains, Interactions hôte-pathogène, Lignée cellulaire, Réplication virale, Tolérance immunitaire, Transcriptome.
English descriptors
- KwdEn :
- MESH :
- immunology : Epithelial Cells.
- isolation & purification : Coronavirus.
- pathogenicity : Coronavirus.
- physiology : Coronavirus.
- virology : Epithelial Cells, Severe Acute Respiratory Syndrome.
- Cell Line, Host-Pathogen Interactions, Humans, Immune Tolerance, Transcriptome, Virus Replication.
Abstract
A novel human coronavirus (HCoV-EMC) was recently identified in the Middle East as the causative agent of a severe acute respiratory syndrome (SARS) resembling the illness caused by SARS coronavirus (SARS-CoV). Although derived from the CoV family, the two viruses are genetically distinct and do not use the same receptor. Here, we investigated whether HCoV-EMC and SARS-CoV induce similar or distinct host responses after infection of a human lung epithelial cell line. HCoV-EMC was able to replicate as efficiently as SARS-CoV in Calu-3 cells and similarly induced minimal transcriptomic changes before 12 h postinfection. Later in infection, HCoV-EMC induced a massive dysregulation of the host transcriptome, to a much greater extent than SARS-CoV. Both viruses induced a similar activation of pattern recognition receptors and the interleukin 17 (IL-17) pathway, but HCoV-EMC specifically down-regulated the expression of several genes within the antigen presentation pathway, including both type I and II major histocompatibility complex (MHC) genes. This could have an important impact on the ability of the host to mount an adaptive host response. A unique set of 207 genes was dysregulated early and permanently throughout infection with HCoV-EMC, and was used in a computational screen to predict potential antiviral compounds, including kinase inhibitors and glucocorticoids. Overall, HCoV-EMC and SARS-CoV elicit distinct host gene expression responses, which might impact in vivo pathogenesis and could orient therapeutic strategies against that emergent virus.
DOI: 10.1128/mBio.00165-13
PubMed: 23631916
Affiliations:
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Le document en format XML
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Although derived from the CoV family, the two viruses are genetically distinct and do not use the same receptor. Here, we investigated whether HCoV-EMC and SARS-CoV induce similar or distinct host responses after infection of a human lung epithelial cell line. HCoV-EMC was able to replicate as efficiently as SARS-CoV in Calu-3 cells and similarly induced minimal transcriptomic changes before 12 h postinfection. Later in infection, HCoV-EMC induced a massive dysregulation of the host transcriptome, to a much greater extent than SARS-CoV. Both viruses induced a similar activation of pattern recognition receptors and the interleukin 17 (IL-17) pathway, but HCoV-EMC specifically down-regulated the expression of several genes within the antigen presentation pathway, including both type I and II major histocompatibility complex (MHC) genes. This could have an important impact on the ability of the host to mount an adaptive host response. A unique set of 207 genes was dysregulated early and permanently throughout infection with HCoV-EMC, and was used in a computational screen to predict potential antiviral compounds, including kinase inhibitors and glucocorticoids. Overall, HCoV-EMC and SARS-CoV elicit distinct host gene expression responses, which might impact in vivo pathogenesis and could orient therapeutic strategies against that emergent virus.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><noCountry><name sortKey="Agnihothram, Sudhakar" sort="Agnihothram, Sudhakar" uniqKey="Agnihothram S" first="Sudhakar" last="Agnihothram">Sudhakar Agnihothram</name><name sortKey="Baric, Ralph S" sort="Baric, Ralph S" uniqKey="Baric R" first="Ralph S" last="Baric">Ralph S. Baric</name><name sortKey="Carter, Victoria S" sort="Carter, Victoria S" uniqKey="Carter V" first="Victoria S" last="Carter">Victoria S. Carter</name><name sortKey="Graham, Rachel L" sort="Graham, Rachel L" uniqKey="Graham R" first="Rachel L" last="Graham">Rachel L. Graham</name><name sortKey="Gralinski, Lisa E" sort="Gralinski, Lisa E" uniqKey="Gralinski L" first="Lisa E" last="Gralinski">Lisa E. Gralinski</name><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G" last="Katze">Michael G. Katze</name><name sortKey="Menachery, Vineet D" sort="Menachery, Vineet D" uniqKey="Menachery V" first="Vineet D" last="Menachery">Vineet D. Menachery</name><name sortKey="Sova, Pavel" sort="Sova, Pavel" uniqKey="Sova P" first="Pavel" last="Sova">Pavel Sova</name><name sortKey="Yount, Boyd L" sort="Yount, Boyd L" uniqKey="Yount B" first="Boyd L" last="Yount">Boyd L. Yount</name></noCountry><country name="États-Unis"><region name="Washington (État)"><name sortKey="Josset, Laurence" sort="Josset, Laurence" uniqKey="Josset L" first="Laurence" last="Josset">Laurence Josset</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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