Dengue fever is caused by DENV 1–4 serotypes transmitted by Aedes mosquitoes. Secondary infection with a different serotype leads to severe dengue (dengue haemorrhagic fever/DSS). The primary immunopathological mechanism of plasma leakage in severe dengue is:
- A Direct NS1 glycoprotein-mediated complement fixation and lysis of vascular endothelium
- B Th2 cytokine-mediated eosinophil degranulation on endothelium
- C Antibody-dependent enhancement (ADE) causing hyperactivation of monocytes/macrophages with cytokine storm ✓
- D Platelet aggregation forming microthrombi in capillaries
Explanation
In secondary dengue infection with a heterologous serotype, pre-existing non-neutralising IgG antibodies from the primary infection bind the new serotype, forming immune complexes that are taken up by Fc receptor–bearing monocytes/macrophages at a much higher rate. This antibody-dependent enhancement (ADE) results in massive viral replication in these cells and a cytokine storm (TNF-α, IL-6, IL-8, IFN-γ), leading to increased vascular permeability, plasma leakage, and thrombocytopaenia. NS1 contributes to coagulopathy by cross-reacting with platelet and endothelial antigens, but ADE is the primary pathogenic mechanism for severe dengue.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.