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
2011 Impact Factor: 3.363
2011 SCImago Journal Rankings: 0.360
DOIhttp://dx.doi.org/10.1099/vir.0.82619-0
ISI Accession Number IDWOS:000247087900018
ReferencesReferences in Scopus
DC Field
Value
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
dc.identifier.hkuros133519
dc.identifier.isiWOS:000247087900018
dc.identifier.issn0022-1317
2011 Impact Factor: 3.363
2011 SCImago Journal Rankings: 0.360
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
Author Affiliations
  1. The University of Hong Kong