scholarly journals 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

2014 ◽  
Vol 89 (4) ◽  
pp. 2013-2023 ◽  
Author(s):  
Yuet Wu ◽  
Wenwei Tu ◽  
Kwok-Tai Lam ◽  
Kin-Hung Chow ◽  
Pak-Leung Ho ◽  
...  
Keyword(s):  
Influenza Virus ◽  
B Cells ◽  
Virus Infection ◽  
B Cell ◽  
Cell Response ◽  
Plasma Cells ◽  
Pneumococcal Infection ◽  
Influenza Virus Infection ◽  
Follicular Helper ◽  
B Cell Response

ABSTRACTSecondaryStreptococcus pneumoniaeinfection 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.IMPORTANCESecondary pneumococcal infection after influenza virus infection is an important clinical issue that often results in excess mortality. Since antibodies are key mediators of protection, this study aims to examine the antibody response to influenza virus and demonstrates that lethal coinfection reduced the B cell response to influenza virus. This study helps to highlight the complexity of the modulation of the B cell response in the context of coinfection.

Role of the B-cell response in recovery of mice from primary influenza virus infection

1997 ◽  
Vol 159 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Walter Gerhard ◽  
Krystyna Mozdzanowska ◽  
Michelle Furchner ◽  
George Washko ◽  
Krista Maiese
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
B Cell ◽  
Cell Response ◽  
Influenza Virus Infection ◽  
B Cell Response

scholarly journals Influenza Virus Infection Causes Global Respiratory Tract B Cell Response Modulation via Innate Immune Signals

2007 ◽  
Vol 178 (3) ◽  
pp. 1457-1467 ◽  
Author(s):  
W. L. William Chang ◽  
Elizabeth S. Coro ◽  
Friederike C. Rau ◽  
Yuanyuan Xiao ◽  
David J. Erle ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Respiratory Tract ◽  
B Cell ◽  
Cell Response ◽  
Influenza Virus Infection ◽  
Innate Immune ◽  
Response Modulation ◽  
B Cell Response

scholarly journals A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection

2011 ◽  
Vol 8 (6) ◽  
pp. 462-468 ◽  
Author(s):  
Xiaohui Wang ◽  
Chris CS Chan ◽  
Min Yang ◽  
Jun Deng ◽  
Vincent KM Poon ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
B Cell ◽  
Cell Response ◽  
Critical Role ◽  
Influenza Virus Infection ◽  
H5n1 Influenza Virus ◽  
H5n1 Influenza ◽  
B Cell Response

scholarly journals Broad Hemagglutinin-Specific Memory B Cell Expansion by Seasonal Influenza Virus Infection Reflects Early-Life Imprinting and Adaptation to the Infecting Virus

2019 ◽  
Vol 93 (8) ◽  
Author(s):  
Brenda L. Tesini ◽  
Preshetha Kanagaiah ◽  
Jiong Wang ◽  
Megan Hahn ◽  
Jessica L. Halliley ◽  
...  
Keyword(s):  
Influenza Virus ◽  
B Cells ◽  
Virus Infection ◽  
B Cell ◽  
Specific Antibody ◽  
Early Life ◽  
Influenza Virus Infection ◽  
Memory B Cells ◽  
Specific Memory ◽  
Original Antigenic Sin

ABSTRACTMemory B cells (MBCs) are key determinants of the B cell response to influenza virus infection and vaccination, but the effect of different forms of influenza antigen exposure on MBC populations has received little attention. We analyzed peripheral blood mononuclear cells and plasma collected following human H3N2 influenza infection to investigate the relationship between hemagglutinin-specific antibody production and changes in the size and character of hemagglutinin-reactive MBC populations. Infection produced increased concentrations of plasma IgG reactive to the H3 head of the infecting virus, to the conserved stalk, and to a broad chronological range of H3s consistent with original antigenic sin responses. H3-reactive IgG MBC expansion after infection included reactivity to head and stalk domains. Notably, expansion of H3 head-reactive MBC populations was particularly broad and reflected original antigenic sin patterns of IgG production. Findings also suggest that early-life H3N2 infection “imprints” for strong H3 stalk-specific MBC expansion. Despite the breadth of MBC expansion, the MBC response included an increase in affinity for the H3 head of the infecting virus. Overall, our findings indicate that H3-reactive MBC expansion following H3N2 infection is consistent with maintenance of response patterns established early in life, but nevertheless includes MBC adaptation to the infecting virus.IMPORTANCERapid and vigorous virus-specific antibody responses to influenza virus infection and vaccination result from activation of preexisting virus-specific memory B cells (MBCs). Understanding the effects of different forms of influenza virus exposure on MBC populations is therefore an important guide to the development of effective immunization strategies. We demonstrate that exposure to the influenza hemagglutinin via natural infection enhances broad protection through expansion of hemagglutinin-reactive MBC populations that recognize head and stalk regions of the molecule. Notably, we show that hemagglutinin-reactive MBC expansion reflects imprinting by early-life infection and that this might apply to stalk-reactive, as well as to head-reactive, MBCs. Our findings provide experimental support for the role of MBCs in maintaining imprinting effects and suggest a mechanism by which imprinting might confer heterosubtypic protection against avian influenza viruses. It will be important to compare our findings to the situation after influenza vaccination.

scholarly journals B-Cell Response during Protozoan Parasite Infections

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
María C. Amezcua Vesely ◽  
Daniela A. Bermejo ◽  
Carolina L. Montes ◽  
Eva V. Acosta-Rodríguez ◽  
Adriana Gruppi
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Response ◽  
Plasma Cells ◽  
Protozoan Parasite ◽  
Parasite Infections ◽  
Protozoan Infections ◽  
Induced Apoptosis ◽  
Cellular Immune ◽  
B Cell Response

In this review, we discuss how protozoan parasites alter immature and mature B cell compartment. B1 and marginal zone (MZ) B cells, considered innate like B cells, are activated during protozoan parasite infections, and they generate short lived plasma cells providing a prompt antibody source. In addition, protozoan infections induce massive B cell response with polyclonal activation that leads to hypergammaglobulnemia with serum antibodies specific for the parasites and self and/or non related antigens. To protect themselves, the parasites have evolved unique ways to evade B cell immune responses inducing apoptosis of MZ and conventional mature B cells. As a consequence of the parasite induced-apoptosis, the early IgM response and an already establish humoral immunity are affected during the protozoan parasite infection. Moreover, some trypanosomatides trigger bone marrow immature B cell apoptosis, influencing the generation of new mature B cells. Simultaneously with their ability to release antibodies, B cells produce cytokines/quemokines that influence the characteristic of cellular immune response and consequently the progression of parasite infections.

scholarly journals High Preexisting Serological Antibody Levels Correlate with Diversification of the Influenza Vaccine Response

2015 ◽  
Vol 89 (6) ◽  
pp. 3308-3317 ◽  
Author(s):  
Sarah F. Andrews ◽  
Kaval Kaur ◽  
Noel T. Pauli ◽  
Min Huang ◽  
Yunping Huang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
B Cells ◽  
Influenza Vaccine ◽  
B Cell ◽  
Cell Response ◽  
Vaccine Response ◽  
Trivalent Influenza Vaccine ◽  
Antibody Levels ◽  
Virus Strains ◽  
B Cell Response

ABSTRACTReactivation of memory B cells allows for a rapid and robust immune response upon challenge with the same antigen. Variant influenza virus strains generated through antigenic shift or drift are encountered multiple times over the lifetime of an individual. One might predict, then, that upon vaccination with the trivalent influenza vaccine across multiple years, the antibody response would become more and more dominant toward strains consistently present in the vaccine at the expense of more divergent strains. However, when we analyzed the vaccine-induced plasmablast, memory, and serological responses to the trivalent influenza vaccine between 2006 and 2013, we found that the B cell response was most robust against more divergent strains. Overall, the antibody response was highest when one or more strains contained in the vaccine varied from year to year. This suggests that in the broader immunological context of viral antigen exposure, the B cell response to variant influenza virus strains is not dictated by the composition of the memory B cell precursor pool. The outcome is instead a diversified B cell response.IMPORTANCEVaccine strategies are being designed to boost broadly reactive B cells present in the memory repertoire to provide universal protection to the influenza virus. It is important to understand how past exposure to influenza virus strains affects the response to subsequent immunizations. The viral epitopes targeted by B cells responding to the vaccine may be a direct reflection of the B cell memory specificities abundant in the preexisting immune repertoire, or other factors may influence the vaccine response. Here, we demonstrate that high preexisting serological antibody levels to a given influenza virus strain correlate with low production of antibody-secreting cells and memory B cells recognizing that strain upon revaccination. In contrast, introduction of antigenically novel strains generates a robust B cell response. Thus, both the preexisting memory B cell repertoire and serological antibody levels must be taken into consideration in predicting the quality of the B cell response to new prime-boost vaccine strategies.

scholarly journals Broadly cross-reactive antibodies dominate the human B cell response against 2009 pandemic H1N1 influenza virus infection

2011 ◽  
Vol 208 (2) ◽  
pp. 411-411 ◽  
Author(s):  
Jens Wrammert ◽  
Dimitrios Koutsonanos ◽  
Gui-Mei Li ◽  
Srilatha Edupuganti ◽  
Jianhua Sui ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
B Cell ◽  
Cell Response ◽  
Influenza Virus Infection ◽  
H1n1 Influenza ◽  
Pandemic H1n1 ◽  
H1n1 Influenza Virus ◽  
Pandemic H1n1 Influenza ◽  
Human B Cell
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