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BCG-Vaccinated Children with Contact to Tuberculosis Patients Show Delayed Conversion of Mycobacterium
Dorcas O Owusu1, Ernest Adankwah1,2, Wilfred Aniagyei1
1Kumasi Centre for Collaborative Research in Tropical Medicine (KCCR), Kumasi 00233, Ghana.
Insights
BCG vaccination in babies may delay immune responses to tuberculosis (TB) infection, showing lower initial IFN-γ levels but balanced responses over time. These findings suggest BCG vaccination impacts TB-specific T-cell phenotypes.
Area of Science:
- Immunology
- Infectious Diseases
- Public Health
Background:
- BCG vaccination is recommended for infants in high TB prevalence countries like Ghana.
- While BCG protects against severe TB, its effect on IFN-γ induction post-Mycobacterium tuberculosis infection is understudied.
Purpose of the Study:
- To investigate the impact of BCG vaccination on IFN-γ production and T-cell responses in children exposed to M. tuberculosis.
- To identify potential immune biomarkers for protection against severe TB manifestations.
Main Methods:
- IFN-γ Release Assay (IGRA) and T-cell activation marker assay (TAM-TB) were used.
- Children with TB contact were divided into BCG-vaccinated (n=77) and non-BCG-vaccinated (n=17) groups.
- Immune responses were assessed at baseline, 3 months, and 12 months.
Main Results:
- BCG-vaccinated children showed lower initial IFN-γ levels and IGRA positivity compared to non-vaccinated contacts.
- Immune conversion and IFN-γ expression balanced between groups by month 12.
- Non-BCG-vaccinated children had higher IFN-γ+ T-cells and transient CD38+ T-cells.
Conclusions:
- BCG vaccination appears to induce delayed immune conversion and distinct T-cell phenotypes in contacts of TB patients.
- These BCG-induced immune differences may serve as biomarkers for protection against severe clinical TB.
Abstract:
Mycobacterium (M.) bovis BCG vaccination is recommended for healthy babies after birth in several countries with a high prevalence of tuberculosis, including Ghana. Previous studies showed that BCG vaccination prevents individuals from developing severe clinical manifestations of tuberculosis, but BCG vaccination effects on the induction of IFN-γ after M. tuberculosis infection have hardly been investigated. Here, we performed IFN-γ-based T-cell assays (i.e., IFN-γ Release Assay, IGRA; T-cell activation and maturation marker assay, TAM-TB) in children who had contact with index tuberculosis patients (contacts). These contacts were classified as either being BCG vaccinated at birth (n = 77) or non-BCG-vaccinated (n = 17) and were followed up at three timepoints for a period of one year to determine immune conversion after M. tuberculosis exposure and potential infection. At baseline and month 3, BCG-vaccinated contacts had significantly lower IFN-γ levels after stimulation with M. tuberculosis-specific proteins as compared to non-BCG-vaccinated contacts. This resulted in decreased proportions of positive IGRA results (BCG-vaccinated: 60% at baseline, 57% at month 3; non-BCG-vaccinated: 77% and 88%, respectively) at month 3. However, until month 12, immune conversion in BCG-vaccinated contacts led to balanced proportions in IGRA responders and IFN-γ expression between the study groups. TAM-TB assay analyses confirmed higher proportions of IFN-γ-positive T-cells in non-BCG-vaccinated contacts. Low proportions of CD38-positive M. tuberculosis-specific T-cells were only detected in non-BCG-vaccinated contacts at baseline. These results suggest that BCG vaccination causes delayed immune conversion as well as differences in the phenotype of M. tuberculosis-specific T-cells in BCG-vaccinated contacts of tuberculosis patients. These differences are immune biomarker candidates for protection against the development of severe clinical tuberculosis manifestations.
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