In severe dengue, which pathophysiological mechanism directly explains the development of plasma leakage and dengue shock syndrome?
- A Antibody-dependent enhancement (ADE) causing immune complex-mediated complement activation and massive cytokine release increasing vascular permeability ✓
- B Direct viral cytopathic destruction of endothelial cells
- C Disseminated intravascular coagulation as the primary cause of hypovolaemia
- D Dengue NS1 protein-mediated platelet destruction
Explanation
In secondary dengue infection with a heterologous serotype, pre-existing cross-reactive non-neutralising IgG antibodies facilitate viral uptake into FcR-bearing monocytes/macrophages (antibody-dependent enhancement, ADE). This leads to markedly increased viral replication and activation of T cells and macrophages, producing a cytokine storm (TNF-α, IL-6, IL-8, IFN-γ) that increases endothelial permeability — the hallmark of dengue shock syndrome. Direct viral endothelial destruction is minimal. DIC occurs but is secondary to shock, not primary. NS1-mediated platelet destruction contributes to thrombocytopenia but is not the primary mechanism of plasma leakage.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.