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COMPARATIVE STUDY
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Impaired Bacillus Calmette-Guérin cellular immune response in HIV-exposed, uninfected infants.
AIDS 2011 November 14
OBJECTIVE: To evaluate cell-mediated immune response to Bacillus Calmette-Guérin (BCG) vaccination in uninfected, HIV-1-exposed infants, comparing it with unexposed children.
DESIGN: It is designed as a cross-sectional study.
METHODS: BCG-specific lymphoproliferation and T-cell subsets (CD4(+), CD8(+) and TCR γδ(+)) by flow cytometry and interleukin-10, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) concentration by ELISA were analyzed in HIV-exposed and unexposed infants. Whole blood lymphocyte immunophenotyping and blood counts were performed in exposed children. Nonparametric tests were used (P < 0.05).
RESULTS: Given the ontogeny of the immune system, exposed infants were separated into three groups according to age: exposed 1 (E1, aged 6.1-8.8 months), E2 (aged 9.1-17.1 months) and E3 (aged 18.1-26.3 months). Unexposed infants (UE group) and E1 were matched for age. Cell proliferation was not different among the three exposed groups, neither for BCG nor for phytohemagglutinin (PHA)-stimulated cultures. Furthermore, BCG-stimulated lymphoproliferation was reduced in the E1 group in comparison with the UE group. T-lymphocyte subpopulations also showed differences, with the youngest HIV-exposed groups (E1 and E2) showing a predominant proliferation of CD4(+) T cells in cultures with BCG, whereas E3 and UE groups had a robust γδ(+) T-cell expansion. There was lower IFN-γ concentration in the samples from E1 group in comparison with all of the other groups. The unexposed infants showed higher TNF-α concentration in cultures with BCG and PHA in comparison with E1 group.
CONCLUSION: BCG-specific T-cell proliferation was reduced in HIV-exposed uninfected infants and IFN-γ concentration was lower in younger exposed infants, showing a delay in immune system maturation of HIV-exposed infants.
DESIGN: It is designed as a cross-sectional study.
METHODS: BCG-specific lymphoproliferation and T-cell subsets (CD4(+), CD8(+) and TCR γδ(+)) by flow cytometry and interleukin-10, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) concentration by ELISA were analyzed in HIV-exposed and unexposed infants. Whole blood lymphocyte immunophenotyping and blood counts were performed in exposed children. Nonparametric tests were used (P < 0.05).
RESULTS: Given the ontogeny of the immune system, exposed infants were separated into three groups according to age: exposed 1 (E1, aged 6.1-8.8 months), E2 (aged 9.1-17.1 months) and E3 (aged 18.1-26.3 months). Unexposed infants (UE group) and E1 were matched for age. Cell proliferation was not different among the three exposed groups, neither for BCG nor for phytohemagglutinin (PHA)-stimulated cultures. Furthermore, BCG-stimulated lymphoproliferation was reduced in the E1 group in comparison with the UE group. T-lymphocyte subpopulations also showed differences, with the youngest HIV-exposed groups (E1 and E2) showing a predominant proliferation of CD4(+) T cells in cultures with BCG, whereas E3 and UE groups had a robust γδ(+) T-cell expansion. There was lower IFN-γ concentration in the samples from E1 group in comparison with all of the other groups. The unexposed infants showed higher TNF-α concentration in cultures with BCG and PHA in comparison with E1 group.
CONCLUSION: BCG-specific T-cell proliferation was reduced in HIV-exposed uninfected infants and IFN-γ concentration was lower in younger exposed infants, showing a delay in immune system maturation of HIV-exposed infants.
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