Article: Wild type and mutant 2009 pandemic influenza A (H1N1) viruses cause more severe disease and higher mortality in pregnant BALB/c mice
| Title | Wild type and mutant 2009 pandemic influenza A (H1N1) viruses cause more severe disease and higher mortality in pregnant BALB/c mice | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Authors | Chan, 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 Date | 2010 | ||||||||
| Publisher | Public 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?] DOI: http://dx.doi.org/10.1371/journal.pone.0013757 | ||||||||
| 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. © 2010 Chan et al. | ||||||||
| ISSN | 1932-6203 2011 Impact Factor: 4.092 2011 SCImago Journal Rankings: 0.519 | ||||||||
| DOI | http://dx.doi.org/10.1371/journal.pone.0013757 | ||||||||
| ISI Accession Number ID | WOS:000283645300036
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 ID | PMC2966430 | ||||||||
| References | References in Scopus |
| dc.contributor.author | Chan, KH | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| dc.contributor.author | Zhang, AJX | ||||||||
| dc.contributor.author | To, KKW | ||||||||
| dc.contributor.author | Chan, CCS | ||||||||
| dc.contributor.author | Poon, VKM | ||||||||
| dc.contributor.author | Guo, K | ||||||||
| dc.contributor.author | Ng, F | ||||||||
| dc.contributor.author | Zhang, QW | ||||||||
| dc.contributor.author | Leung, VHC | ||||||||
| dc.contributor.author | Cheung, ANY | ||||||||
| dc.contributor.author | Lau, CCY | ||||||||
| dc.contributor.author | Woo, PCY | ||||||||
| dc.contributor.author | Tse, H | ||||||||
| dc.contributor.author | Wu, W | ||||||||
| dc.contributor.author | Chen, H | ||||||||
| dc.contributor.author | Zheng, BJ | ||||||||
| dc.contributor.author | Yuen, KY | ||||||||
| dc.date.accessioned | 2011-07-27T01:30:46Z | ||||||||
| dc.date.available | 2011-07-27T01:30:46Z | ||||||||
| dc.date.issued | 2010 | ||||||||
| dc.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. © 2010 Chan et al. | ||||||||
| dc.description.nature | published_or_final_version | ||||||||
| dc.identifier.citation | Plos One, 2010, v. 5 n. 10 [How to Cite?] DOI: http://dx.doi.org/10.1371/journal.pone.0013757 | ||||||||
| dc.identifier.doi | http://dx.doi.org/10.1371/journal.pone.0013757 | ||||||||
| dc.identifier.epage | e13757 | ||||||||
| dc.identifier.hkuros | 187081 | ||||||||
| dc.identifier.isi | WOS:000283645300036
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.issn | 1932-6203 2011 Impact Factor: 4.092 2011 SCImago Journal Rankings: 0.519 | ||||||||
| dc.identifier.issue | 10 | ||||||||
| dc.identifier.pmcid | PMC2966430 | ||||||||
| dc.identifier.pmid | 21060798 | ||||||||
| dc.identifier.scopus | eid_2-s2.0-78149450826 | ||||||||
| dc.identifier.spage | e13757 | ||||||||
| dc.identifier.uri | http://hdl.handle.net/10722/135257 | ||||||||
| dc.identifier.volume | 5 | ||||||||
| dc.language | eng | ||||||||
| dc.publisher | Public Library of Science. The Journal's web site is located at http://www.plosone.org/home.action | ||||||||
| dc.publisher.place | United States | ||||||||
| dc.relation.ispartof | PLoS ONE | ||||||||
| dc.relation.references | References in Scopus | ||||||||
| dc.rights | Creative Commons: Attribution 3.0 Hong Kong License | ||||||||
| dc.subject.mesh | Antibodies, Viral - biosynthesis | ||||||||
| dc.subject.mesh | Influenza A Virus, H1N1 Subtype - genetics - isolation and purification - physiology | ||||||||
| dc.subject.mesh | Mutation | ||||||||
| dc.subject.mesh | Orthomyxoviridae Infections - immunology - mortality - physiopathology - virology | ||||||||
| dc.subject.mesh | T-Lymphocytes - immunology | ||||||||
| dc.title | Wild type and mutant 2009 pandemic influenza A (H1N1) viruses cause more severe disease and higher mortality in pregnant BALB/c mice | ||||||||
| dc.type | Article |
- The University of Hong Kong

