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Article: Lethal coinfection of influenza virus and Streptococcus pneumoniae lowers antibody response to influenza virus in lung and reduces numbers of germinal center B cells, T follicular helper cells, and plasma cells in mediastinal lymph Node

TitleLethal coinfection of influenza virus and Streptococcus pneumoniae lowers antibody response to influenza virus in lung and reduces numbers of germinal center B cells, T follicular helper cells, and plasma cells in mediastinal lymph Node
Authors
Issue Date2015
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal of Virology, 2015, v. 89 n. 4, p. 2013-2023 How to Cite?
AbstractSecondary Streptococcus pneumoniae infection after influenza is a significant clinical complication resulting in morbidity and sometimes mortality. Prior influenza virus infection has been demonstrated to impair the macrophage and neutrophil response to the subsequent pneumococcal infection. In contrast, how a secondary pneumococcal infection after influenza can affect the adaptive immune response to the initial influenza virus infection is less well understood. Therefore, this study focuses on how secondary pneumococcal infection after influenza may impact the humoral immune response to the initial influenza virus infection in a lethal coinfection mouse model. Compared to mice infected with influenza virus alone, mice coinfected with influenza virus followed by pneumococcus had significant body weight loss and 100% mortality. In the lung, lethal coinfection significantly increased virus titers and bacterial cell counts and decreased the level of virus-specific IgG, IgM, and IgA, as well as the number of B cells, CD4 T cells, and plasma cells. Lethal coinfection significantly reduced the size and weight of spleen, as well as the number of B cells along the follicular developmental lineage. In mediastinal lymph nodes, lethal coinfection significantly decreased germinal center B cells, T follicular helper cells, and plasma cells. Adoptive transfer of influenza virus-specific immune serum to coinfected mice improved survival, suggesting the protective functions of anti-influenza virus antibodies. In conclusion, coinfection reduced the B cell response to influenza virus. This study helps us to understand the modulation of the B cell response to influenza virus during a lethal coinfection.
Persistent Identifierhttp://hdl.handle.net/10722/209410
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWu, Y-
dc.contributor.authorTu, W-
dc.contributor.authorLam, KT-
dc.contributor.authorChow, KH-
dc.contributor.authorHo, PL-
dc.contributor.authorGuan, Y-
dc.contributor.authorPeiris, JSM-
dc.contributor.authorLau, YL-
dc.date.accessioned2015-04-17T05:15:46Z-
dc.date.available2015-04-17T05:15:46Z-
dc.date.issued2015-
dc.identifier.citationJournal of Virology, 2015, v. 89 n. 4, p. 2013-2023-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/209410-
dc.description.abstractSecondary Streptococcus pneumoniae infection after influenza is a significant clinical complication resulting in morbidity and sometimes mortality. Prior influenza virus infection has been demonstrated to impair the macrophage and neutrophil response to the subsequent pneumococcal infection. In contrast, how a secondary pneumococcal infection after influenza can affect the adaptive immune response to the initial influenza virus infection is less well understood. Therefore, this study focuses on how secondary pneumococcal infection after influenza may impact the humoral immune response to the initial influenza virus infection in a lethal coinfection mouse model. Compared to mice infected with influenza virus alone, mice coinfected with influenza virus followed by pneumococcus had significant body weight loss and 100% mortality. In the lung, lethal coinfection significantly increased virus titers and bacterial cell counts and decreased the level of virus-specific IgG, IgM, and IgA, as well as the number of B cells, CD4 T cells, and plasma cells. Lethal coinfection significantly reduced the size and weight of spleen, as well as the number of B cells along the follicular developmental lineage. In mediastinal lymph nodes, lethal coinfection significantly decreased germinal center B cells, T follicular helper cells, and plasma cells. Adoptive transfer of influenza virus-specific immune serum to coinfected mice improved survival, suggesting the protective functions of anti-influenza virus antibodies. In conclusion, coinfection reduced the B cell response to influenza virus. This study helps us to understand the modulation of the B cell response to influenza virus during a lethal coinfection.-
dc.languageeng-
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/-
dc.relation.ispartofJournal of Virology-
dc.rightsJournal of Virology. Copyright © American Society for Microbiology.-
dc.titleLethal coinfection of influenza virus and Streptococcus pneumoniae lowers antibody response to influenza virus in lung and reduces numbers of germinal center B cells, T follicular helper cells, and plasma cells in mediastinal lymph Node-
dc.typeArticle-
dc.identifier.emailWu, Y: wuzoe@hku.hk-
dc.identifier.emailTu, W: wwtu@hku.hk-
dc.identifier.emailLam, KT: tailam@hkucc.hku.hk-
dc.identifier.emailChow, KH: khchowb@hku.hk-
dc.identifier.emailHo, PL: plho@hkucc.hku.hk-
dc.identifier.emailGuan, Y: yguan@hkucc.hku.hk-
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hk-
dc.identifier.emailLau, YL: lauylung@hku.hk-
dc.identifier.authorityTu, W=rp00416-
dc.identifier.authorityChow, KH=rp00370-
dc.identifier.authorityHo, PL=rp00406-
dc.identifier.authorityGuan, Y=rp00397-
dc.identifier.authorityPeiris, JSM=rp00410-
dc.identifier.authorityLau, YL=rp00361-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.02455-14-
dc.identifier.pmcidPMC4338877-
dc.identifier.scopuseid_2-s2.0-84921695376-
dc.identifier.hkuros242823-
dc.identifier.volume89-
dc.identifier.issue4-
dc.identifier.spage2013-
dc.identifier.epage2023-
dc.identifier.isiWOS:000348562800008-
dc.publisher.placeUnited States-

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