Post-Dengue Syndrome: From Immunopathogenesis to Multisystemic Clinical Sequelae

Dengue virus (DENV) causes the most prevalent arboviral infection worldwide. Alt-hough classically regarded as an acute illness, growing evidence describes Post-Dengue Syndrome (PDS) as a chronic entity with profound sequelae. This narrative review an-alyzes its pathophysiology: the cytokine storm, antibody-dependent enhancement, and NS1-triggered molecular mimicry, together with the cells that execute them—dendritic cells, mononuclear phagocytes, NK cells, platelets, and complement on the innate side; plasmablast expansion, follicular helper T cell activation, defective regulatory control, and PD-L1/PD-1-mediated exhaustion on the adaptive side. Genetic susceptibility is examined through polymorphisms of HLA, FcγRIIa, Toll-like receptor, and cytokine genes. Multisystemic manifestations are described—persistent fatigue, fibromyal-gia-like myalgia and arthralgia, alopecia, brain fog, and mood disturbance—alongside neurological complications, categorized into direct neuroinvasion and post-infectious immune-mediated damage such as Guillain-Barré syndrome and encephalomyelitis. Recent population-based data linking dengue to acute neurological events and to later cognitive decline are examined critically, as is the unsettled question of whether post-dengue neuroinflammation amounts to neurodegeneration. Finally, the influence of age and sex is addressed, and therapeutic and research priorities are outlined, of-fering an immunoclinical perspective for the multidisciplinary management of these patients.