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Immunophenotype Expressions and Cytokine Profiles of Influenza A H1N1 Virus Infection in Pediatric Patients in 2009
Author(s) -
Shih-Min Wang,
Yu-Ting Liao,
Yu-Shiang Hu,
TzongShiann Ho,
ChingFen Shen,
JenRen Wang,
Yee-Shin Lin,
Ching-Chuan Liu
Publication year - 2014
Publication title -
disease markers
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 66
eISSN - 1875-8630
pISSN - 0278-0240
DOI - 10.1155/2014/195453
Subject(s) - immunophenotyping , cytokine storm , medicine , immunology , cytokine , immune system , peripheral blood mononuclear cell , virus , influenza a virus , cd8 , pathogenesis , flow cytometry , biology , covid-19 , in vitro , biochemistry , disease , infectious disease (medical specialty)
Background . A novel swine-origin influenza A H1N1 virus (S-OIV) caused human infection and acute respiratory illness in 2009, resulting in an influenza pandemic. Objectives . This study characterized the immune responses of S-OIV infection in pediatric patients at risk of pulmonary complications. Methods . All enrolled pediatric patients were confirmed virologically for S-OIV infection in 2009-2010, prospectively. Changes in cellular immunophenotypes were analyzed using flow cytometry. Plasma cytokine levels associated with S-OIV infection by pulmonary and without pulmonary complications were measured using cytokine cytometric bead assay kits. Results . A total of 85 patients with a mean age of 10.3 years were recruited. The level of C-reactive protein (CRP) was high in patients exhibiting pulmonary complications. The percentage of cellular immunophenotypes did not change between patients with and without pulmonary complications. The absolute numbers of peripheral blood mononuclear cells (PBMC), CD3, CD8, and CD16CD56 decreased with acute S-OIV pulmonary complications. Acute influenza infection with pulmonary complications was associated with high plasma concentrations of IL-1 β , IL-6, IL-12, and IFN- γ . Conclusion . Immunophenotype studies have reported variability in immune response to the severity of S-OIV infections. Acute phase cytokine profiles of the 2009 S-OIV infection might have contributed to the pathogenesis of the pulmonary complications.

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