Imunopatomekanisme Demam Berdarah Dengue (DHF)

Abstract

Dengue Hemorrhagic Fever (DHF) represents a severe manifestation of dengue virus infection, primarily driven by complex immune dysregulation during secondary heterologous infections. This review synthesizes current knowledge on DHF immunopathogenesis, emphasizing Antibody-Dependent Enhancement (ADE), T-cell cross-reactivity, cytokine storms, and hemostatic disturbances. Key mechanisms include ADE-mediated viral entry into monocytes/macrophages, aberrant T-cell responses ("original antigenic sin"), and endothelial damage from inflammatory cytokines (TNF-α, IL-6). These processes trigger plasma leakage (hematocrit ↑>20%), thrombocytopenia (<100,000/μL), and coagulopathy. Risk factors include secondary infection (15–80× increased risk), DENV-2/DENV-3 serotypes, and host genetics. Early detection of hemoconcentration and thrombocytopenia remains critical. Immunomodulatory therapies and multiserotype vaccines represent promising interventions informed by these mechanisms