Article: Wild type and mutant 2009 pandemic influenza A (H1N1) viruses cause more severe disease and higher mortality in pregnant BALB/c mice

File Download Links for fulltext
(May Require Subscription)
Supplementary
  • Basic View
  • Metadata View
  • XML View
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
2011 Impact Factor: 4.092
2011 SCImago Journal Rankings: 0.519
DOIhttp://dx.doi.org/10.1371/journal.pone.0013757
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.

PubMed Central IDPMC2966430
ReferencesReferences in Scopus
DC Field
Value
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
2011 Impact Factor: 4.092
2011 SCImago Journal Rankings: 0.519
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
Author Affiliations
  1. The University of Hong Kong