ArticleBMC infectious diseases2026
The HIF-1α-Th17/Treg axis in pediatric infectious mononucleosis: a clinical investigation of metabolic-immune dysregulation.
Article in BMC infectious diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPediatric infectious mononucleosis (IM) is a systemic inflammatory syndrome typically triggered by primary Epstein-Barr virus (EBV) infection. The disease is characterized by a profound disruption of immune homeostasis, which can be characterized by the balance between pro-inflammatory Th17 cells and suppressive Treg cells. While hypoxia-inducible factor-1α (HIF-1α) is known to direct T-cell behavior in various inflammatory conditions, its specific role in the immunopathology of IM remains largely uncharacterized. This study aims to investigate the systemic expression of HIF-1α in pediatric IM and evaluate its correlation with the Th17/Treg homeostatic axis.
methodsIn this prospective case-control study, we enrolled pediatric patients with acute IM and healthy, age- and sex-frequency-matched controls. Peripheral blood CD4
resultsThe final analysis included 40 IM patients and 37 healthy controls. Compared to the controls, IM patients exhibited a significant systemic accumulation of HIF-1α (p < 0.001) and IL-17A concentrations (p = 0.008), alongside a marked expansion of Th17 cells (p < 0.001) and a significant increase in the Th17/Treg ratio (p < 0.001). Conversely, the IM cohort experienced significantly depletions in Treg frequencies (p < 0.001) and TGF-β1 levels (p = 0.005). Correlation analysis revealed that serum HIF-1α was correlated significantly positively with Th17 frequency, the Th17/Treg ratio, and IL-17A levels and significantly negatively with Treg frequency and TGF-β1 levels.
conclusionsOur findings reveal a significant systemic stabilization of HIF-1α in pediatric IM patients, which reflects an immunometabolic signature associated with the acute viral response. The significant correlation between HIF-1α and the shift in T-cell subsets suggests that HIF-1α may be seen as systemic sensor of disease severity in EBV infection. The results provide a theoretical foundation for targeting metabolic pathways to restore immune homeostasis in hyper-inflammatory viral diseases.
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