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Article: Tropism and innate host responses of a novel avian influenza A H7N9 virus: an analysis of ex-vivo and in-vitro cultures of the human respiratory tract

TitleTropism and innate host responses of a novel avian influenza A H7N9 virus: an analysis of ex-vivo and in-vitro cultures of the human respiratory tract
Authors
Issue Date2013
PublisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/journals/the-lancet-respiratory-medicine/2213-2600
Citation
The Lancet Respiratory Medicine, 2013, v. 1 n. 7, p. 534-542 How to Cite?
AbstractBACKGROUND: Since March, 2013, an avian-origin influenza A H7N9 virus has caused severe pneumonia in China. The aim of this study was to investigate the pathogenesis of this new virus in human beings. METHODS: We obtained ex-vivo cultures of the human bronchus, lung, nasopharynx, and tonsil and in-vitro cultures of primary human alveolar epithelial cells and peripheral blood monocyte-derived macrophages. We compared virus tropism and induction of proinflammatory cytokine responses of two human influenza A H7N9 virus isolates, A/Shanghai/1/2013 and A/Shanghai/2/2013; a highly pathogenic avian influenza H5N1 virus; the highly pathogenic avian influenza H7N7 virus that infected human beings in the Netherlands in 2003; the 2009 pandemic influenza H1N1 virus, and a low pathogenic duck H7N9 virus that was genetically different to the human disease causing A H7N9 viruses. FINDINGS: Both human H7N9 viruses replicated efficiently in human bronchus and lung ex-vivo cultures, whereas duck/H7N9 virus failed to replicate in either. Both human A H7N9 viruses infected both ciliated and non-ciliated human bronchial epithelial cells and replicated to higher titres than did H5N1 (p<0·0001 to 0·0046) and A/Shanghai/1/2013 replicated to higher titres than did H7N7 (p=0·0002-0·01). Both human A H7N9 viruses predominantly infected type II alveolar epithelial cells and alveolar macrophages in the human lung and replicated to higher titres than did H5N1 (p<0·0001 to 0·0078); A/Shanghai/1/2013 replicated to higher titres than did H1N1 (p=0·0052-0·05) and H7N7 (p=0·0031-0·0151). Human H7N9 viruses were less potent inducers of proinflammatory cytokines compared with H5N1 virus. INTERPRETATION: Collectively, the results suggest that the novel H7N9 viruses are better adapted to infect and replicate in the human conducting and lower airways than are other avian influenza viruses, including H5N1, and pose an important pandemic threat.
Persistent Identifierhttp://hdl.handle.net/10722/194836
ISSN
2015 Impact Factor: 15.328
2015 SCImago Journal Rankings: 5.252
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, MCWen_US
dc.contributor.authorChan, WYen_US
dc.contributor.authorChan, LYen_US
dc.contributor.authorMok, KPen_US
dc.contributor.authorHui, PYen_US
dc.contributor.authorFong, JHMen_US
dc.contributor.authorTao, KPen_US
dc.contributor.authorPoon, LLMen_US
dc.contributor.authorNicholls, JMen_US
dc.contributor.authorGuan, Yen_US
dc.contributor.authorPeiris, JSMen_US
dc.date.accessioned2014-02-17T02:14:42Z-
dc.date.available2014-02-17T02:14:42Z-
dc.date.issued2013en_US
dc.identifier.citationThe Lancet Respiratory Medicine, 2013, v. 1 n. 7, p. 534-542en_US
dc.identifier.issn2213-2600-
dc.identifier.urihttp://hdl.handle.net/10722/194836-
dc.description.abstractBACKGROUND: Since March, 2013, an avian-origin influenza A H7N9 virus has caused severe pneumonia in China. The aim of this study was to investigate the pathogenesis of this new virus in human beings. METHODS: We obtained ex-vivo cultures of the human bronchus, lung, nasopharynx, and tonsil and in-vitro cultures of primary human alveolar epithelial cells and peripheral blood monocyte-derived macrophages. We compared virus tropism and induction of proinflammatory cytokine responses of two human influenza A H7N9 virus isolates, A/Shanghai/1/2013 and A/Shanghai/2/2013; a highly pathogenic avian influenza H5N1 virus; the highly pathogenic avian influenza H7N7 virus that infected human beings in the Netherlands in 2003; the 2009 pandemic influenza H1N1 virus, and a low pathogenic duck H7N9 virus that was genetically different to the human disease causing A H7N9 viruses. FINDINGS: Both human H7N9 viruses replicated efficiently in human bronchus and lung ex-vivo cultures, whereas duck/H7N9 virus failed to replicate in either. Both human A H7N9 viruses infected both ciliated and non-ciliated human bronchial epithelial cells and replicated to higher titres than did H5N1 (p<0·0001 to 0·0046) and A/Shanghai/1/2013 replicated to higher titres than did H7N7 (p=0·0002-0·01). Both human A H7N9 viruses predominantly infected type II alveolar epithelial cells and alveolar macrophages in the human lung and replicated to higher titres than did H5N1 (p<0·0001 to 0·0078); A/Shanghai/1/2013 replicated to higher titres than did H1N1 (p=0·0052-0·05) and H7N7 (p=0·0031-0·0151). Human H7N9 viruses were less potent inducers of proinflammatory cytokines compared with H5N1 virus. INTERPRETATION: Collectively, the results suggest that the novel H7N9 viruses are better adapted to infect and replicate in the human conducting and lower airways than are other avian influenza viruses, including H5N1, and pose an important pandemic threat.en_US
dc.languageengen_US
dc.publisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/journals/the-lancet-respiratory-medicine/2213-2600-
dc.relation.ispartofThe Lancet Respiratory Medicineen_US
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in The Lancet Respiratory Medicine. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in The Lancet Respiratory Medicine, 2013, v. 1 n. 7, p. 534-542. DOI: 10.1016/S2213-2600(13)70138-3-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleTropism and innate host responses of a novel avian influenza A H7N9 virus: an analysis of ex-vivo and in-vitro cultures of the human respiratory tracten_US
dc.typeArticleen_US
dc.identifier.emailChan, MCW: mchan@hku.hken_US
dc.identifier.emailChan, WY: reneewy@hku.hken_US
dc.identifier.emailChan, LY: louisa12@hku.hken_US
dc.identifier.emailMok, KP: ch02mkp@hkucc.hku.hken_US
dc.identifier.emailHui, PY: kenrie@hkucc.hku.hken_US
dc.identifier.emailFong, JHM: fongjhm@hku.hken_US
dc.identifier.emailTao, KP: marstao@hku.hken_US
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_US
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hken_US
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hken_US
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_US
dc.identifier.authorityChan, MCW=rp00420en_US
dc.identifier.authorityChan, WY=rp01596en_US
dc.identifier.authorityMok, KP=rp01805en_US
dc.identifier.authorityPoon, LLM=rp00484en_US
dc.identifier.authorityNicholls, JM=rp00364en_US
dc.identifier.authorityGuan, Y=rp00397en_US
dc.identifier.authorityPeiris, JSM=rp00410en_US
dc.description.naturepostprint-
dc.identifier.doi10.1016/S2213-2600(13)70138-3en_US
dc.identifier.pmid24461614-
dc.identifier.hkuros227935en_US
dc.identifier.hkuros217207-
dc.identifier.volume1en_US
dc.identifier.issue7-
dc.identifier.spage534en_US
dc.identifier.epage542en_US
dc.identifier.isiWOS:000342690100018-
dc.publisher.placeUnited Kingdom-

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