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Article: Cellular response to influenza virus infection: A potential role for autophagy in CXCL10 and interferon-alpha induction
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TitleCellular response to influenza virus infection: A potential role for autophagy in CXCL10 and interferon-alpha induction
 
AuthorsLaw, AHY1
Lee, DCW1
Yuen, KY1
Peiris, M1
Lau, ASY1
 
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
 
CitationCellular And Molecular Immunology, 2010, v. 7 n. 4, p. 263-270 [How to Cite?]
DOI: http://dx.doi.org/10.1038/cmi.2010.25
 
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.
 
ISSN1672-7681
2013 Impact Factor: 4.185
 
DOIhttp://dx.doi.org/10.1038/cmi.2010.25
 
ISI Accession Number IDWOS:000279487500005
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).

 
ReferencesReferences in Scopus
 
GrantsControl of Pandemic and Inter-pandemic Influenza
Cellular response to influenza virus infection: effect of autophagy versus apoptosis on virus replication
Pathogenesis, cell signaling and virus evolution of avian influenza A (H5N1)
 
DC FieldValue
dc.contributor.authorLaw, AHY
 
dc.contributor.authorLee, DCW
 
dc.contributor.authorYuen, KY
 
dc.contributor.authorPeiris, M
 
dc.contributor.authorLau, ASY
 
dc.date.accessioned2010-10-31T13:34:16Z
 
dc.date.available2010-10-31T13:34:16Z
 
dc.date.issued2010
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationCellular And Molecular Immunology, 2010, v. 7 n. 4, p. 263-270 [How to Cite?]
DOI: http://dx.doi.org/10.1038/cmi.2010.25
 
dc.identifier.citeulike9903765
 
dc.identifier.doihttp://dx.doi.org/10.1038/cmi.2010.25
 
dc.identifier.epage270
 
dc.identifier.hkuros179327
 
dc.identifier.isiWOS:000279487500005
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).

 
dc.identifier.issn1672-7681
2013 Impact Factor: 4.185
 
dc.identifier.issue4
 
dc.identifier.openurl
 
dc.identifier.pmid20473322
 
dc.identifier.scopuseid_2-s2.0-77957284249
 
dc.identifier.spage263
 
dc.identifier.urihttp://hdl.handle.net/10722/127588
 
dc.identifier.volume7
 
dc.languageeng
 
dc.publisherChinese Society of Immunology. The Journal's web site is located at http://www.nature.com/cmi/index.html
 
dc.publisher.placeChina
 
dc.relation.ispartofCellular and Molecular Immunology
 
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.relation.referencesReferences in Scopus
 
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.subjectautophagy
 
dc.subjectCXCL10
 
dc.subjectinfluenza
 
dc.subjectinterferon
 
dc.titleCellular response to influenza virus infection: A potential role for autophagy in CXCL10 and interferon-alpha induction
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine