The communication between chikungunya infection and the central nervous system

Chikungunya virus (CHIKV) infection is primarily characterized by arthralgia, a persistent joint pain that can significantly impair quality of life. This symptom is linked to the inflammatory processes triggered by the virus. CHIKV infection progresses through acute, subacute, and chronic phases, with increased inflammation correlating to prolonged arthralgia and a poorer prognosis. Emerging evidence suggests that this inflammatory cascade may also play a role in neurological disorders. Neurological complications associated with CHIKV infection include encephalitis, optic neuritis, myeloradiculitis, and Guillain-Barré syndrome (GBS). When CHIKV accesses the central nervous system (CNS), it may do so either directly or through a "Trojan horse" mechanism, activating pro-inflammatory cytokine release and receptors such as HMGB1, P63, and STAR3, which amplify inflammation. This immune response in the CNS is similar to that seen in various neurological conditions, including autism, cerebral palsy, depression, Alzheimer's disease, and neuromyelitis optica. While research into CHIKV's systemic effects has grown, its impact on the CNS and potential role in neurodegenerative diseases remains underexplored. This review aims to fill this gap by examining the links between CHIKV infection and CNS involvement, underscoring the need for further investigation into its contribution to neurological outcomes.