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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

TitleWild type and mutant 2009 pandemic influenza A (H1N1) viruses cause more severe disease and higher mortality in pregnant BALB/c mice
Authors
Issue Date2010
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2010, v. 5 n. 10 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/135257
ISSN
2023 Impact Factor: 2.9
2023 SCImago Journal Rankings: 0.839
PubMed Central ID
ISI Accession Number ID
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.

References

 

DC FieldValueLanguage
dc.contributor.authorChan, KHen_HK
dc.contributor.authorZhang, AJXen_HK
dc.contributor.authorTo, KKWen_HK
dc.contributor.authorChan, CCSen_HK
dc.contributor.authorPoon, VKMen_HK
dc.contributor.authorGuo, Ken_HK
dc.contributor.authorNg, Fen_HK
dc.contributor.authorZhang, QWen_HK
dc.contributor.authorLeung, VHCen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorLau, CCYen_HK
dc.contributor.authorWoo, PCYen_HK
dc.contributor.authorTse, Hen_HK
dc.contributor.authorWu, Wen_HK
dc.contributor.authorChen, Hen_HK
dc.contributor.authorZheng, BJen_HK
dc.contributor.authorYuen, KYen_HK
dc.date.accessioned2011-07-27T01:30:46Z-
dc.date.available2011-07-27T01:30:46Z-
dc.date.issued2010en_HK
dc.identifier.citationPlos One, 2010, v. 5 n. 10en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/135257-
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.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International 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 miceen_HK
dc.typeArticleen_HK
dc.identifier.emailZhang, AJX:zhangajx@hkucc.hku.hken_HK
dc.identifier.emailTo, KKW:kelvinto@hkucc.hku.hken_HK
dc.identifier.emailCheung, ANY:anycheun@hkucc.hku.hken_HK
dc.identifier.emailWoo, PCY:pcywoo@hkucc.hku.hken_HK
dc.identifier.emailTse, H:herman@graduate.hku.hken_HK
dc.identifier.emailChen, H:hlchen@hkucc.hku.hken_HK
dc.identifier.emailZheng, BJ:bzheng@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_HK
dc.identifier.authorityZhang, AJX=rp00413en_HK
dc.identifier.authorityTo, KKW=rp01384en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityWoo, PCY=rp00430en_HK
dc.identifier.authorityTse, H=rp00519en_HK
dc.identifier.authorityChen, H=rp00383en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0013757en_HK
dc.identifier.pmid21060798-
dc.identifier.pmcidPMC2966430-
dc.identifier.scopuseid_2-s2.0-78149450826en_HK
dc.identifier.hkuros187081en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78149450826&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.issue10en_HK
dc.identifier.spagee13757en_US
dc.identifier.epagee13757en_US
dc.identifier.isiWOS:000283645300036-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, KH=7406034307en_HK
dc.identifier.scopusauthoridZhang, AJX=12752135600en_HK
dc.identifier.scopusauthoridTo, KKW=14323807300en_HK
dc.identifier.scopusauthoridChan, CCS=16021156900en_HK
dc.identifier.scopusauthoridPoon, VKM=54934161900en_HK
dc.identifier.scopusauthoridGuo, K=25623179500en_HK
dc.identifier.scopusauthoridNg, F=7103125273en_HK
dc.identifier.scopusauthoridZhang, QW=36912956800en_HK
dc.identifier.scopusauthoridLeung, VHC=36612082100en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridLau, CCY=8398162900en_HK
dc.identifier.scopusauthoridWoo, PCY=7201801340en_HK
dc.identifier.scopusauthoridTse, H=7006070596en_HK
dc.identifier.scopusauthoridWu, W=36912997500en_HK
dc.identifier.scopusauthoridChen, H=26643315400en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.issnl1932-6203-

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