ReviewFrontiers in immunology2026
Immunopathological mechanisms and targeted intervention strategies for chronic chikungunya arthritis: from viral persistence to autoimmunity.
Review in Frontiers in immunology, 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
Chronic chikungunya arthritis (CCA) is a major long-term sequela of Chikungunya virus (CHIKV) infection. Its pathogenesis involves persistent viral reservoirs in joint tissues, metabolic reprogramming of myeloid cells, dysregulated Treg/Th17 immunity, and autoimmune-like tissue injury. This review integrates recent advances in virology, immunometabolism, and clinical pathology to propose a four-stage pathological cascade: "viral persistence", "myeloid metabolic dysregulation", "Treg/Th17 imbalance", and "autoimmunity-like injury". Key cytokine networks and molecular interactions at each stage are summarized. Based on this model, we outline stage-specific therapeutic strategies, including antiviral agents targeting Mxra8 or nsP1 (Stage I), metabolic modulators such as HIF-1α inhibitors and IL-1β blockade (Stage II), immune-restorative therapies such as low-dose IL-2 and CTLA-4-Ig (Stage III), and anti-inflammatory biologics or DMARDs for RA-like pathology (Stage IV). This framework provides a mechanistic basis for precision intervention and supports the development of biomarkers and clinical trial designs for CCA.
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