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Article: Risk assessment of the tropism & pathogenesis of the highly pathogenic avian influenza A/H7N9 virus using ex vivo & in vitro cultures of human respiratory tract.

TitleRisk assessment of the tropism & pathogenesis of the highly pathogenic avian influenza A/H7N9 virus using ex vivo & in vitro cultures of human respiratory tract.
Authors
Keywordsalveolar epithelial cells
H7N9
HPAI
influenza
risk assessment
Issue Date2019
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
The Journal of Infectious Diseases, 2019, v. 220, p. 578-588 How to Cite?
AbstractBackground Highly pathogenic avian influenza (HPAI)-H7N9 virus arising from low pathogenic avian influenza (LPAI)-H7N9 virus with polybasic amino acid substitutions in the hemagglutinin was detected in 2017. Methods We compared the tropism, replication competence, and cytokine induction of HPAI-H7N9, LPAI-H7N9, and HPAI-H5N1 in ex vivo human respiratory tract explants, in vitro culture of human alveolar epithelial cells (AECs) and pulmonary microvascular endothelial cells (HMVEC-L). Results Replication competence of HPAI- and LPAI-H7N9 were comparable in ex vivo cultures of bronchus and lung. HPAI-H7N9 predominantly infected AECs, whereas limited infection was observed in bronchus. The reduced tropism of HPAI-H7N9 in bronchial epithelium may explain the lack of human-to-human transmission despite a number of mammalian adaptation markers. Apical and basolateral release of virus was observed only in HPAI-H7N9- and H5N1-infected AECs regardless of infection route. HPAI-H7N9, but not LPAI-H7N9 efficiently replicated in HMVEC-L. Conclusions Our findings demonstrate that a HPAI-H7N9 virus efficiently replicating in ex vivo cultures of human bronchus and lung. The HPAI-H7N9 was more efficient at replicating in human AECs and HMVEC-L than LPAI-H7N9 implying that endothelial tropism may involve in pathogenesis of HPAI-H7N9 disease.
Persistent Identifierhttp://hdl.handle.net/10722/274504
ISSN
2017 Impact Factor: 5.186
2015 SCImago Journal Rankings: 4.000

 

DC FieldValueLanguage
dc.contributor.authorChan, LY-
dc.contributor.authorHui, PY-
dc.contributor.authorKuok, IT-
dc.contributor.authorBui, HT-
dc.contributor.authorNg, KC-
dc.contributor.authorMok, KP-
dc.contributor.authorYang, Z-
dc.contributor.authorGuan, W-
dc.contributor.authorPoon, LML-
dc.contributor.authorZhong, N-
dc.contributor.authorPeiris, JSM-
dc.contributor.authorNicholls, JM-
dc.contributor.authorChan, MCW-
dc.date.accessioned2019-08-18T15:02:59Z-
dc.date.available2019-08-18T15:02:59Z-
dc.date.issued2019-
dc.identifier.citationThe Journal of Infectious Diseases, 2019, v. 220, p. 578-588-
dc.identifier.issn0022-1899-
dc.identifier.urihttp://hdl.handle.net/10722/274504-
dc.description.abstractBackground Highly pathogenic avian influenza (HPAI)-H7N9 virus arising from low pathogenic avian influenza (LPAI)-H7N9 virus with polybasic amino acid substitutions in the hemagglutinin was detected in 2017. Methods We compared the tropism, replication competence, and cytokine induction of HPAI-H7N9, LPAI-H7N9, and HPAI-H5N1 in ex vivo human respiratory tract explants, in vitro culture of human alveolar epithelial cells (AECs) and pulmonary microvascular endothelial cells (HMVEC-L). Results Replication competence of HPAI- and LPAI-H7N9 were comparable in ex vivo cultures of bronchus and lung. HPAI-H7N9 predominantly infected AECs, whereas limited infection was observed in bronchus. The reduced tropism of HPAI-H7N9 in bronchial epithelium may explain the lack of human-to-human transmission despite a number of mammalian adaptation markers. Apical and basolateral release of virus was observed only in HPAI-H7N9- and H5N1-infected AECs regardless of infection route. HPAI-H7N9, but not LPAI-H7N9 efficiently replicated in HMVEC-L. Conclusions Our findings demonstrate that a HPAI-H7N9 virus efficiently replicating in ex vivo cultures of human bronchus and lung. The HPAI-H7N9 was more efficient at replicating in human AECs and HMVEC-L than LPAI-H7N9 implying that endothelial tropism may involve in pathogenesis of HPAI-H7N9 disease.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org-
dc.relation.ispartofThe Journal of Infectious Diseases-
dc.rightsPre-print: Journal Title] ©: [year] [owner as specified on the article] Published by Oxford University Press [on behalf of xxxxxx]. All rights reserved. Pre-print (Once an article is published, preprint notice should be amended to): This is an electronic version of an article published in [include the complete citation information for the final version of the Article as published in the print edition of the Journal.] Post-print: This is a pre-copy-editing, author-produced PDF of an article accepted for publication in [insert journal title] following peer review. The definitive publisher-authenticated version [insert complete citation information here] is available online at: xxxxxxx [insert URL that the author will receive upon publication here].-
dc.subjectalveolar epithelial cells-
dc.subjectH7N9-
dc.subjectHPAI-
dc.subjectinfluenza-
dc.subjectrisk assessment-
dc.titleRisk assessment of the tropism & pathogenesis of the highly pathogenic avian influenza A/H7N9 virus using ex vivo & in vitro cultures of human respiratory tract.-
dc.typeArticle-
dc.identifier.emailHui, PY: kenrie@hku.hk-
dc.identifier.emailKuok, IT: dkuok@hku.hk-
dc.identifier.emailBui, HT: clyyee@hku.hk-
dc.identifier.emailNg, KC: kckachun@hku.hk-
dc.identifier.emailMok, KP: ch02mkp@hkucc.hku.hk-
dc.identifier.emailPoon, LML: llmpoon@hkucc.hku.hk-
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hk-
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hk-
dc.identifier.emailChan, MCW: mchan@hku.hk-
dc.identifier.authorityHui, PY=rp02149-
dc.identifier.authorityMok, KP=rp01805-
dc.identifier.authorityPoon, LML=rp00484-
dc.identifier.authorityPeiris, JSM=rp00410-
dc.identifier.authorityNicholls, JM=rp00364-
dc.identifier.authorityChan, MCW=rp00420-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/infdis/jiz165-
dc.identifier.hkuros301281-
dc.identifier.volume220-
dc.identifier.spage578-
dc.identifier.epage588-
dc.publisher.placeUnited States-

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