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Article: Screening of differentially expressed transcripts in infectious bursal disease virus-induced apoptotic chicken embryonic fibroblasts by using cDNA microarrays
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TitleScreening of differentially expressed transcripts in infectious bursal disease virus-induced apoptotic chicken embryonic fibroblasts by using cDNA microarrays
 
AuthorsWong, RTY1
Hon, CC1
Zeng, F1
Leung, FCC1
 
Issue Date2007
 
PublisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
 
CitationJournal Of General Virology, 2007, v. 88 n. 6, p. 1785-1796 [How to Cite?]
DOI: http://dx.doi.org/10.1099/vir.0.82619-0
 
AbstractInfectious bursal disease virus (IBDV) induces apoptosis and immunosuppression. To understand the molecular mechanisms involved in the pathogenesis of infectious bursal disease (IBD) and the host-directed antiviral responses, cDNA microarrays were used to identify the differentially expressed transcripts in IBDV-infected chicken embryonic fibroblasts. The results suggest a general suppression of surface receptors, including CD40 ligand and SEMA4D. These are related to T- and B-cell activation and differentiation, which may contribute to the immunosuppression of IBD. In addition, activation of genes involved in Toll-like receptor- and interferon (IFN)-mediated antiviral responses was detected. In particular, upregulation of Toll-like receptor 3, a double-stranded (ds) RNA receptor, and MX1, an IFN-inducible antiviral GTPase, may represent the possible host-directed defence responses against the virus and its dsRNA genome. Interestingly, several lines of evidence suggest the modulation of G protein-coupled receptors and receptor tyrosine kinase signalling pathways, especially the possible transactivation of epidermal growth factor receptor by lysophosphatidic acid. Alteration of these may contribute to the previously reported activation of mitogen-activated protein kinases upon IBDV infection, resulting in macrophage activation and inflammatory responses. Additionally, numerous target genes and inducers of nuclear factor kappa B(NF-κB) were upregulated profoundly, implying that IBDV may modulate host-cell survival and apoptosis to support its replication and facilitate viral spread through NF-κB activation. In summary, this investigation of host-gene expression unravelled the candidate physiological pathways involved in host-virus interaction on a molecular level, providing a foundation for researchers to design experiments based on testable hypotheses targeting individual genes. © 2007 SGM.
 
ISSN0022-1317
2012 Impact Factor: 3.127
2012 SCImago Journal Rankings: 1.245
 
DOIhttp://dx.doi.org/10.1099/vir.0.82619-0
 
ISI Accession Number IDWOS:000247087900018
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWong, RTY
 
dc.contributor.authorHon, CC
 
dc.contributor.authorZeng, F
 
dc.contributor.authorLeung, FCC
 
dc.date.accessioned2010-09-06T09:55:14Z
 
dc.date.available2010-09-06T09:55:14Z
 
dc.date.issued2007
 
dc.description.abstractInfectious bursal disease virus (IBDV) induces apoptosis and immunosuppression. To understand the molecular mechanisms involved in the pathogenesis of infectious bursal disease (IBD) and the host-directed antiviral responses, cDNA microarrays were used to identify the differentially expressed transcripts in IBDV-infected chicken embryonic fibroblasts. The results suggest a general suppression of surface receptors, including CD40 ligand and SEMA4D. These are related to T- and B-cell activation and differentiation, which may contribute to the immunosuppression of IBD. In addition, activation of genes involved in Toll-like receptor- and interferon (IFN)-mediated antiviral responses was detected. In particular, upregulation of Toll-like receptor 3, a double-stranded (ds) RNA receptor, and MX1, an IFN-inducible antiviral GTPase, may represent the possible host-directed defence responses against the virus and its dsRNA genome. Interestingly, several lines of evidence suggest the modulation of G protein-coupled receptors and receptor tyrosine kinase signalling pathways, especially the possible transactivation of epidermal growth factor receptor by lysophosphatidic acid. Alteration of these may contribute to the previously reported activation of mitogen-activated protein kinases upon IBDV infection, resulting in macrophage activation and inflammatory responses. Additionally, numerous target genes and inducers of nuclear factor kappa B(NF-κB) were upregulated profoundly, implying that IBDV may modulate host-cell survival and apoptosis to support its replication and facilitate viral spread through NF-κB activation. In summary, this investigation of host-gene expression unravelled the candidate physiological pathways involved in host-virus interaction on a molecular level, providing a foundation for researchers to design experiments based on testable hypotheses targeting individual genes. © 2007 SGM.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of General Virology, 2007, v. 88 n. 6, p. 1785-1796 [How to Cite?]
DOI: http://dx.doi.org/10.1099/vir.0.82619-0
 
dc.identifier.doihttp://dx.doi.org/10.1099/vir.0.82619-0
 
dc.identifier.epage1796
 
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dc.identifier.isiWOS:000247087900018
 
dc.identifier.issn0022-1317
2012 Impact Factor: 3.127
2012 SCImago Journal Rankings: 1.245
 
dc.identifier.issue6
 
dc.identifier.openurl
 
dc.identifier.pmid17485540
 
dc.identifier.scopuseid_2-s2.0-34249819944
 
dc.identifier.spage1785
 
dc.identifier.urihttp://hdl.handle.net/10722/89309
 
dc.identifier.volume88
 
dc.languageeng
 
dc.publisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofJournal of General Virology
 
dc.relation.referencesReferences in Scopus
 
dc.titleScreening of differentially expressed transcripts in infectious bursal disease virus-induced apoptotic chicken embryonic fibroblasts by using cDNA microarrays
 
dc.typeArticle
 
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<description.abstract>Infectious bursal disease virus (IBDV) induces apoptosis and immunosuppression. To understand the molecular mechanisms involved in the pathogenesis of infectious bursal disease (IBD) and the host-directed antiviral responses, cDNA microarrays were used to identify the differentially expressed transcripts in IBDV-infected chicken embryonic fibroblasts. The results suggest a general suppression of surface receptors, including CD40 ligand and SEMA4D. These are related to T- and B-cell activation and differentiation, which may contribute to the immunosuppression of IBD. In addition, activation of genes involved in Toll-like receptor- and interferon (IFN)-mediated antiviral responses was detected. In particular, upregulation of Toll-like receptor 3, a double-stranded (ds) RNA receptor, and MX1, an IFN-inducible antiviral GTPase, may represent the possible host-directed defence responses against the virus and its dsRNA genome. Interestingly, several lines of evidence suggest the modulation of G protein-coupled receptors and receptor tyrosine kinase signalling pathways, especially the possible transactivation of epidermal growth factor receptor by lysophosphatidic acid. Alteration of these may contribute to the previously reported activation of mitogen-activated protein kinases upon IBDV infection, resulting in macrophage activation and inflammatory responses. Additionally, numerous target genes and inducers of nuclear factor kappa B(NF-&#954;B) were upregulated profoundly, implying that IBDV may modulate host-cell survival and apoptosis to support its replication and facilitate viral spread through NF-&#954;B activation. In summary, this investigation of host-gene expression unravelled the candidate physiological pathways involved in host-virus interaction on a molecular level, providing a foundation for researchers to design experiments based on testable hypotheses targeting individual genes. &#169; 2007 SGM.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong