Dengue hemorrhagic fever (DHF) is more severe during secondary infection with a different dengue serotype. The immunopathological mechanism is:
- A Original antigenic sin causing high-affinity primary antibody response against the new serotype
- B Type III hypersensitivity due to immune complex deposition in dermal capillaries
- C Cytotoxic T cells specific for the primary serotype causing bystander killing of endothelial cells
- D Antibody-Dependent Enhancement (ADE) — sub-neutralizing cross-reactive IgG facilitates virus entry into FcγR-bearing monocytes/macrophages ✓
Explanation
In ADE, cross-reactive non-neutralizing IgG from the primary dengue infection opsonizes heterologous serotype virions; these antibody-virus complexes bind FcγRII on monocytes/macrophages via the Fc region, dramatically increasing viral entry and replication; the increased viral load plus cytokine storm (TNF-alpha, IL-6) drives plasma leakage and hemorrhage in DHF/DSS. Original antigenic sin refers to preferential recall of primary antibodies against the new antigen (a related concept but not the primary mechanism). Type III hypersensitivity involves IC deposition with complement, not the ADE pathway. CTL bystander killing is minor compared to ADE.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.