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Article: Screening of differentially expressed transcripts in infectious bursal disease virus-induced apoptotic chicken embryonic fibroblasts by using cDNA microarrays

TitleScreening of differentially expressed transcripts in infectious bursal disease virus-induced apoptotic chicken embryonic fibroblasts by using cDNA microarrays
Authors
Issue Date2007
PublisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
Citation
Journal Of General Virology, 2007, v. 88 n. 6, p. 1785-1796 How to Cite?
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-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.
Persistent Identifierhttp://hdl.handle.net/10722/89309
ISSN
2013 Impact Factor: 3.529
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, RTYen_HK
dc.contributor.authorHon, CCen_HK
dc.contributor.authorZeng, Fen_HK
dc.contributor.authorLeung, FCCen_HK
dc.date.accessioned2010-09-06T09:55:14Z-
dc.date.available2010-09-06T09:55:14Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of General Virology, 2007, v. 88 n. 6, p. 1785-1796en_HK
dc.identifier.issn0022-1317en_HK
dc.identifier.urihttp://hdl.handle.net/10722/89309-
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.en_HK
dc.languageengen_HK
dc.publisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.orgen_HK
dc.relation.ispartofJournal of General Virologyen_HK
dc.titleScreening of differentially expressed transcripts in infectious bursal disease virus-induced apoptotic chicken embryonic fibroblasts by using cDNA microarraysen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1317&volume=88&spage=1785&epage=1796&date=2007&atitle=Screening+of+differentially+expressed+transcripts+in+infectious+bursal+disease+virus-induced+apoptotic+chicken+embryonic+fibroblasts+by+using+cDNA+microarraysen_HK
dc.identifier.emailLeung, FCC: fcleung@hkucc.hku.hken_HK
dc.identifier.authorityLeung, FCC=rp00731en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1099/vir.0.82619-0en_HK
dc.identifier.pmid17485540en_HK
dc.identifier.scopuseid_2-s2.0-34249819944en_HK
dc.identifier.hkuros133519en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34249819944&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume88en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1785en_HK
dc.identifier.epage1796en_HK
dc.identifier.isiWOS:000247087900018-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWong, RTY=24759484000en_HK
dc.identifier.scopusauthoridHon, CC=7003617137en_HK
dc.identifier.scopusauthoridZeng, F=7202911544en_HK
dc.identifier.scopusauthoridLeung, FCC=7103078633en_HK

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