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Chikungunya fever (CHIKF), an acute arboviral disease caused by the chikungunya virus (CHIKV), is characterized by fever, debilitating arthralgia, and systemic inflammation, posing a significant public health burden in endemic regions like Guangdong Province, China. The early immunopathological mechanisms following CHIKV infection remain incompletely understood. This prospective cohort study investigated dysregulated effector T cell responses and inflammatory cytokine profiles in 34 patients with acute CHIKF, compared to 20 healthy controls, during a 2025 outbreak in Guangdong. Flow cytometry and multiplex cytokine analysis revealed significant suppression of key effector populations, including CD3 + T cells, CD8 + T cells, and natural killer T (NKT) cells, alongside a marked elevation of pro−inflammatory cytokines IL−1β, IL−6, and IL−8. The degree of T cell dysregulation is closely related to the appearance of clinical symptoms, particularly arthralgia and fever. Furthermore, pre−existing comorbidities and advanced age were associated with more pronounced immune abnormalities. Male patients exhibited a higher risk of inflammatory dysregulation, demonstrated by greater NKT cell depletion and IL−1β upregulation compared to females. Notably, pro−inflammatory cytokine levels strongly correlated with neutrophil counts and systemic inflammatory markers but not with T cell subset alterations, suggesting distinct pathological pathways. These findings delineate a dual immunopathogenic state in acute CHIKV infection, involving concurrent effector T cell suppression and IL-1β-associated inflammatory response, which provides insights into potential biomarkers and therapeutic targets for disease management.
Xiao et al. (Tue,) studied this question.