Genetic damage and immune dysregulation in Schistosoma haematobium-infected individuals in Nigeria.

BACKGROUND

Urogenital schistosomiasis caused by affects over 100 million people globally, with potential long-term genetic and immunological consequences poorly understood in endemic populations. This study investigates genetic damage and immune dysregulation in infected individuals from a hyperendemic region in Nigeria.

OBJECTIVE

To quantify genetic damage markers and characterize immune system alterations in individuals with confirmed infection compared to uninfected controls from Atisbo Local Government Area, Oyo State, Nigeria.

METHODS

This cross-sectional study included 240 participants (120 infected, 120 controls) aged 15–65 years, selected using multi-stage cluster sampling. Genetic damage was assessed using comet assay, micronucleus testing, and chromosomal aberration analysis. Immune profiling included Th1/Th2 cytokines, immunoglobulins, and complement components. Multivariate regression models identified independent predictors of genetic damage.

RESULTS

Infected individuals demonstrated markedly elevated genetic damage: comet tail moment 15.7 ± 4.2 versus 6.3 ± 2.1 (Cohen’s d = 2.80,  < 0.001), micronucleus frequency 8.4 ± 2.7 versus 3.1 ± 1.2 per 1000 cells (d = 2.41,  < 0.001), and chromosomal abnormalities 12.3% versus 4.1% ( < 0.001). Pronounced Th2 polarization was evident with IL-4 increased 4.1-fold, IL-5 4.6-fold, and IL-13 4.1-fold, while IFN-γ was reduced by 65% (all  < 0.001, FDR-adjusted). infection independently predicted genetic damage (β = 8.42, 95% CI: 7.51–9.33,  < 0.001) after adjusting for age, BMI, hemoglobin, and sex, explaining 73% of the variance in tail moment values.

CONCLUSIONS

infection causes substantial genetic damage and Th2-dominant immune dysregulation with potentially serious long-term health consequences. These findings provide scientific justification for intensified control efforts, enhanced post-treatment monitoring, and cancer surveillance programs in endemic populations.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1186/s12865-025-00749-w.