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|Title:||Deteriorating pneumococcal-specific B-cell memory in minimally symptomatic African children with HIV infection|
|Citation:||Journal of Infectious Diseases, 2011; 204(4):534-543|
|Publisher:||Oxford University Press|
|Oluwadamilola H. Iwajomo, Adam Finn, Peter Moons, Rose Nkhata, Enoch Sepako, Abiodun D. Ogunniyi, Neil A. Williams, and Robert S. Heyderman|
|Abstract:||Invasive pneumococcal disease is a leading cause of human immunodeficiency virus (HIV)–associated mortality in sub-Saharan African children. Defective T-cell–mediated immunity partially explains this high disease burden, but there is an increased risk of invasive pneumococcal disease even in the context of a relatively preserved percentage of CD4 cells. We hypothesized that impaired B-cell immunity to this pathogen further amplifies the immune defect. We report a shift in the B-cell compartment toward an apoptosis-prone phenotype evident early in HIV disease progression. We show that, although healthy HIV-uninfected and minimally symptomatic HIV-infected children have similar numbers of isotype-switched memory B cells, numbers of pneumococcal protein antigen–specific memory B cells were lower in HIV-infected than in HIV-uninfected children. Our data implicate defective naturally acquired B-cell pneumococcal immunity in invasive pneumococcal disease causation in HIV-infected children and highlight the need to study the functionality and duration of immune memory to novel pneumococcal protein vaccine candidates in order to optimize their effectiveness in this population.|
CD4 Lymphocyte Count
Immunoglobulin Class Switching
Enzyme-Linked Immunospot Assay
|Rights:||© The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved.|
|Appears in Collections:||Aurora harvest|
Molecular and Biomedical Science publications
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