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Article: Wild type and mutant 2009 pandemic influenza A (H1N1) viruses cause more severe disease and higher mortality in pregnant BALB/c mice
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TitleWild type and mutant 2009 pandemic influenza A (H1N1) viruses cause more severe disease and higher mortality in pregnant BALB/c mice
 
AuthorsChan, KH1
Zhang, AJX1
To, KKW1
Chan, CCS1
Poon, VKM1
Guo, K1
Ng, F1
Zhang, QW1
Leung, VHC1
Cheung, ANY1
Lau, CCY1
Woo, PCY1
Tse, H1
Wu, W1
Chen, H1
Zheng, BJ1
Yuen, KY1
 
Issue Date2010
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPlos One, 2010, v. 5 n. 10 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0013757
 
AbstractBackground: Pregnant women infected by the pandemic influenza A (H1N1) 2009 virus had more severe disease and higher mortality but its pathogenesis is still unclear. Principal Findings: We showed that higher mortality, more severe pneumonitis, higher pulmonary viral load, lower peripheral blood T lymphocytes and antibody responses, higher levels of proinflammatory cytokines and chemokines, and worse fetal development occurred in pregnant mice than non-pregnant controls infected by either wild type (clinical isolate) or mouse-adapted mutant virus with D222G substitution in hemagglutinin. These disease-associated changes and the lower respiratory tract involvement were worse in pregnant mice challenged by mutant virus. Though human placental origin JEG-3 cell line could be infected and proinflammatory cytokines or chemokines were elevated in amniotic fluid of some mice, no placental or fetal involvement by virus were detected by culture, real-time reverse transcription polymerase chain reaction or histopathological changes. Dual immunofluorescent staining of viral nucleoprotein and type II alveolar cell marker SP-C protein suggested that the majority of infected alveolar epithelial cells were type II pneumocytes. Conclusion: The adverse effect of this pandemic virus on maternal and fetal outcome is largely related to the severe pulmonary disease and the indirect effect of inflammatory cytokine spillover into the systemic circulation. © 2010 Chan et al.
 
ISSN1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0013757
 
PubMed Central IDPMC2966430
 
ISI Accession Number IDWOS:000283645300036
Funding AgencyGrant Number
Ted Sun Foundation
Ms. Teresa Wong On Yik, Research Fund for the Control of Infectious Diseases of the Food and Health Bureau
Research Grants Council of the Hong Kong Special Administrative Region, China
Funding Information:

The authors are grateful to the support from the Ted Sun Foundation, the Clinical Infectious Diseases Research Endowment Fund from Ms. Teresa Wong On Yik, Research Fund for the Control of Infectious Diseases of the Food and Health Bureau, and the Research Grants Council of the Hong Kong Special Administrative Region, China. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorChan, KH
 
dc.contributor.authorZhang, AJX
 
dc.contributor.authorTo, KKW
 
dc.contributor.authorChan, CCS
 
dc.contributor.authorPoon, VKM
 
dc.contributor.authorGuo, K
 
dc.contributor.authorNg, F
 
dc.contributor.authorZhang, QW
 
dc.contributor.authorLeung, VHC
 
dc.contributor.authorCheung, ANY
 
dc.contributor.authorLau, CCY
 
dc.contributor.authorWoo, PCY
 
dc.contributor.authorTse, H
 
dc.contributor.authorWu, W
 
dc.contributor.authorChen, H
 
dc.contributor.authorZheng, BJ
 
dc.contributor.authorYuen, KY
 
dc.date.accessioned2011-07-27T01:30:46Z
 
dc.date.available2011-07-27T01:30:46Z
 
dc.date.issued2010
 
dc.description.abstractBackground: Pregnant women infected by the pandemic influenza A (H1N1) 2009 virus had more severe disease and higher mortality but its pathogenesis is still unclear. Principal Findings: We showed that higher mortality, more severe pneumonitis, higher pulmonary viral load, lower peripheral blood T lymphocytes and antibody responses, higher levels of proinflammatory cytokines and chemokines, and worse fetal development occurred in pregnant mice than non-pregnant controls infected by either wild type (clinical isolate) or mouse-adapted mutant virus with D222G substitution in hemagglutinin. These disease-associated changes and the lower respiratory tract involvement were worse in pregnant mice challenged by mutant virus. Though human placental origin JEG-3 cell line could be infected and proinflammatory cytokines or chemokines were elevated in amniotic fluid of some mice, no placental or fetal involvement by virus were detected by culture, real-time reverse transcription polymerase chain reaction or histopathological changes. Dual immunofluorescent staining of viral nucleoprotein and type II alveolar cell marker SP-C protein suggested that the majority of infected alveolar epithelial cells were type II pneumocytes. Conclusion: The adverse effect of this pandemic virus on maternal and fetal outcome is largely related to the severe pulmonary disease and the indirect effect of inflammatory cytokine spillover into the systemic circulation. © 2010 Chan et al.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2010, v. 5 n. 10 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0013757
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0013757
 
dc.identifier.epagee13757
 
dc.identifier.hkuros187081
 
dc.identifier.isiWOS:000283645300036
Funding AgencyGrant Number
Ted Sun Foundation
Ms. Teresa Wong On Yik, Research Fund for the Control of Infectious Diseases of the Food and Health Bureau
Research Grants Council of the Hong Kong Special Administrative Region, China
Funding Information:

The authors are grateful to the support from the Ted Sun Foundation, the Clinical Infectious Diseases Research Endowment Fund from Ms. Teresa Wong On Yik, Research Fund for the Control of Infectious Diseases of the Food and Health Bureau, and the Research Grants Council of the Hong Kong Special Administrative Region, China. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
dc.identifier.issn1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
dc.identifier.issue10
 
dc.identifier.pmcidPMC2966430
 
dc.identifier.pmid21060798
 
dc.identifier.scopuseid_2-s2.0-78149450826
 
dc.identifier.spagee13757
 
dc.identifier.urihttp://hdl.handle.net/10722/135257
 
dc.identifier.volume5
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshAntibodies, Viral - biosynthesis
 
dc.subject.meshInfluenza A Virus, H1N1 Subtype - genetics - isolation and purification - physiology
 
dc.subject.meshMutation
 
dc.subject.meshOrthomyxoviridae Infections - immunology - mortality - physiopathology - virology
 
dc.subject.meshT-Lymphocytes - immunology
 
dc.titleWild type and mutant 2009 pandemic influenza A (H1N1) viruses cause more severe disease and higher mortality in pregnant BALB/c mice
 
dc.typeArticle
 
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<description.abstract>Background: Pregnant women infected by the pandemic influenza A (H1N1) 2009 virus had more severe disease and higher mortality but its pathogenesis is still unclear. Principal Findings: We showed that higher mortality, more severe pneumonitis, higher pulmonary viral load, lower peripheral blood T lymphocytes and antibody responses, higher levels of proinflammatory cytokines and chemokines, and worse fetal development occurred in pregnant mice than non-pregnant controls infected by either wild type (clinical isolate) or mouse-adapted mutant virus with D222G substitution in hemagglutinin. These disease-associated changes and the lower respiratory tract involvement were worse in pregnant mice challenged by mutant virus. Though human placental origin JEG-3 cell line could be infected and proinflammatory cytokines or chemokines were elevated in amniotic fluid of some mice, no placental or fetal involvement by virus were detected by culture, real-time reverse transcription polymerase chain reaction or histopathological changes. Dual immunofluorescent staining of viral nucleoprotein and type II alveolar cell marker SP-C protein suggested that the majority of infected alveolar epithelial cells were type II pneumocytes. Conclusion: The adverse effect of this pandemic virus on maternal and fetal outcome is largely related to the severe pulmonary disease and the indirect effect of inflammatory cytokine spillover into the systemic circulation. &#169; 2010 Chan et al.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong