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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
Title | 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 |
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Authors | |
Issue Date | 2015 |
Publisher | American 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? |
Abstract | Secondary 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 Identifier | http://hdl.handle.net/10722/209410 |
ISSN | 2021 Impact Factor: 6.549 2020 SCImago Journal Rankings: 2.617 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Wu, Y | - |
dc.contributor.author | Tu, W | - |
dc.contributor.author | Lam, KT | - |
dc.contributor.author | Chow, KH | - |
dc.contributor.author | Ho, PL | - |
dc.contributor.author | Guan, Y | - |
dc.contributor.author | Peiris, JSM | - |
dc.contributor.author | Lau, YL | - |
dc.date.accessioned | 2015-04-17T05:15:46Z | - |
dc.date.available | 2015-04-17T05:15:46Z | - |
dc.date.issued | 2015 | - |
dc.identifier.citation | Journal of Virology, 2015, v. 89 n. 4, p. 2013-2023 | - |
dc.identifier.issn | 0022-538X | - |
dc.identifier.uri | http://hdl.handle.net/10722/209410 | - |
dc.description.abstract | Secondary 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.language | eng | - |
dc.publisher | American Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/ | - |
dc.relation.ispartof | Journal of Virology | - |
dc.rights | Journal of Virology. Copyright © American Society for Microbiology. | - |
dc.title | 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 | - |
dc.type | Article | - |
dc.identifier.email | Wu, Y: wuzoe@hku.hk | - |
dc.identifier.email | Tu, W: wwtu@hku.hk | - |
dc.identifier.email | Lam, KT: tailam@hkucc.hku.hk | - |
dc.identifier.email | Chow, KH: khchowb@hku.hk | - |
dc.identifier.email | Ho, PL: plho@hkucc.hku.hk | - |
dc.identifier.email | Guan, Y: yguan@hkucc.hku.hk | - |
dc.identifier.email | Peiris, JSM: malik@hkucc.hku.hk | - |
dc.identifier.email | Lau, YL: lauylung@hku.hk | - |
dc.identifier.authority | Tu, W=rp00416 | - |
dc.identifier.authority | Chow, KH=rp00370 | - |
dc.identifier.authority | Ho, PL=rp00406 | - |
dc.identifier.authority | Guan, Y=rp00397 | - |
dc.identifier.authority | Peiris, JSM=rp00410 | - |
dc.identifier.authority | Lau, YL=rp00361 | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1128/JVI.02455-14 | - |
dc.identifier.pmcid | PMC4338877 | - |
dc.identifier.scopus | eid_2-s2.0-84921695376 | - |
dc.identifier.hkuros | 242823 | - |
dc.identifier.volume | 89 | - |
dc.identifier.issue | 4 | - |
dc.identifier.spage | 2013 | - |
dc.identifier.epage | 2023 | - |
dc.identifier.isi | WOS:000348562800008 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0022-538X | - |