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Article: Cellular response to influenza virus infection: A potential role for autophagy in CXCL10 and interferon-alpha induction

TitleCellular response to influenza virus infection: A potential role for autophagy in CXCL10 and interferon-alpha induction
Authors
Keywordsautophagy
CXCL10
influenza
interferon
Issue Date2010
PublisherChinese Society of Immunology. The Journal's web site is located at http://www.nature.com/cmi/index.html
Citation
Cellular And Molecular Immunology, 2010, v. 7 n. 4, p. 263-270 How to Cite?
Abstract
Historically, influenza pandemics have arisen from avian influenza viruses. Avian influenza viruses H5N1 and H9N2 are potential pandemic candidates. Infection of humans with the highly pathogenic avian influenza H5N1 virus is associated with a mortality in excess of 60%, which has been attributed to dysregulation of the cytokine system. Human macrophages and epithelial cells infected with some genotypes of H5N1 and H9N2 viruses express markedly elevated cytokine and chemokine levels when compared with seasonal influenza A subtype H1N1 virus. The mechanisms underlying this cytokine and chemokine hyperinduction are not fully elucidated. In the present study, we demonstrate that autophagy, a tightly regulated homeostatic process for self-digestion of unwanted cellular subcomponents, plays a role in cytokine induction. Autophagy is induced to a greater extent by H9N2/G1, in association with cytokine hyperinduction, compared with H1N1 and the novel pandemic swine-origin influenza A/H1N1 viruses. Using 3-methyladenine to inhibit autophagy and small interfering RNA to silence the autophagy gene, Atg5, we further show that autophagic responses play a role in influenza virus-induced CXCL10 and interferon-α expression in primary human blood macrophages. Our results provide new insights into the pathogenic mechanisms of avian influenza viruses. © 2010 CSI and USTC. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/127588
ISSN
2013 Impact Factor: 4.185
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong KongAoE/M-12/06
Research Fund for Control of Infectious Disease09080832
Research Grants Council Central AllocationHKU 1/05C
Funding Information:

This work was supported by Area of Excellence grants to Malik Peiris, K. Y. Yuen and Allan S. Lau (Grant AoE/M-12/06) from the Research Grants Council of Hong Kong and the Research Fund for Control of Infectious Disease (09080832), as well as grants to Allan S. Lau and Malik Peiris from the Research Grants Council Central Allocation (HKU 1/05C).

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorLaw, AHYen_HK
dc.contributor.authorLee, DCWen_HK
dc.contributor.authorYuen, KYen_HK
dc.contributor.authorPeiris, Men_HK
dc.contributor.authorLau, ASYen_HK
dc.date.accessioned2010-10-31T13:34:16Z-
dc.date.available2010-10-31T13:34:16Z-
dc.date.issued2010en_HK
dc.identifier.citationCellular And Molecular Immunology, 2010, v. 7 n. 4, p. 263-270en_HK
dc.identifier.issn1672-7681en_HK
dc.identifier.urihttp://hdl.handle.net/10722/127588-
dc.description.abstractHistorically, influenza pandemics have arisen from avian influenza viruses. Avian influenza viruses H5N1 and H9N2 are potential pandemic candidates. Infection of humans with the highly pathogenic avian influenza H5N1 virus is associated with a mortality in excess of 60%, which has been attributed to dysregulation of the cytokine system. Human macrophages and epithelial cells infected with some genotypes of H5N1 and H9N2 viruses express markedly elevated cytokine and chemokine levels when compared with seasonal influenza A subtype H1N1 virus. The mechanisms underlying this cytokine and chemokine hyperinduction are not fully elucidated. In the present study, we demonstrate that autophagy, a tightly regulated homeostatic process for self-digestion of unwanted cellular subcomponents, plays a role in cytokine induction. Autophagy is induced to a greater extent by H9N2/G1, in association with cytokine hyperinduction, compared with H1N1 and the novel pandemic swine-origin influenza A/H1N1 viruses. Using 3-methyladenine to inhibit autophagy and small interfering RNA to silence the autophagy gene, Atg5, we further show that autophagic responses play a role in influenza virus-induced CXCL10 and interferon-α expression in primary human blood macrophages. Our results provide new insights into the pathogenic mechanisms of avian influenza viruses. © 2010 CSI and USTC. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherChinese Society of Immunology. The Journal's web site is located at http://www.nature.com/cmi/index.htmlen_HK
dc.relation.ispartofCellular and Molecular Immunologyen_HK
dc.subjectautophagyen_HK
dc.subjectCXCL10en_HK
dc.subjectinfluenzaen_HK
dc.subjectinterferonen_HK
dc.subject.meshAutophagy - immunology-
dc.subject.meshChemokine CXCL10 - biosynthesis-
dc.subject.meshInfluenza A virus - immunology-
dc.subject.meshInfluenza, Human - immunology - virology-
dc.subject.meshInterferon-alpha - biosynthesis-
dc.titleCellular response to influenza virus infection: A potential role for autophagy in CXCL10 and interferon-alpha inductionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1672-7681&volume=7&issue=4&spage=263&epage=270&date=2010&atitle=Cellular+response+to+influenza+virus+infection:+a+potential+role+for+autophagy+in+CXCL10+and+interferon-alpha+induction-
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hken_HK
dc.identifier.emailPeiris, M: malik@hkucc.hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.identifier.authorityPeiris, M=rp00410en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/cmi.2010.25en_HK
dc.identifier.pmid20473322-
dc.identifier.scopuseid_2-s2.0-77957284249en_HK
dc.identifier.hkuros179327en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77957284249&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue4en_HK
dc.identifier.spage263en_HK
dc.identifier.epage270en_HK
dc.identifier.isiWOS:000279487500005-
dc.publisher.placeChinaen_HK
dc.relation.projectControl of Pandemic and Inter-pandemic Influenza-
dc.relation.projectCellular response to influenza virus infection: effect of autophagy versus apoptosis on virus replication-
dc.relation.projectPathogenesis, cell signaling and virus evolution of avian influenza A (H5N1)-
dc.identifier.scopusauthoridLaw, AHY=8692488400en_HK
dc.identifier.scopusauthoridLee, DCW=15751156000en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.scopusauthoridPeiris, M=7005486823en_HK
dc.identifier.scopusauthoridLau, ASY=7202626202en_HK
dc.identifier.citeulike9903765-

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