In dengue pathogenesis, which immunological mechanism best explains why secondary infection with a heterologous dengue serotype causes more severe disease (dengue haemorrhagic fever/dengue shock syndrome)?

• A Direct viral cytopathic effect causing platelet lysis
• B T-cell exhaustion from persistent viraemia
• C Cross-reactivity between dengue NS1 and endothelial cell surface proteins
• D Antibody-dependent enhancement (ADE) leading to increased viral uptake into mononuclear cells ✓

Explanation

The dominant mechanism in secondary heterologous dengue infection is antibody-dependent enhancement: cross-reactive IgG antibodies from the primary infection bind the new serotype but cannot neutralise it; instead, the virus-antibody complex is internalised via Fc receptors on mononuclear phagocytes, dramatically amplifying viral replication. This drives an exuberant cytokine response ('cytokine storm') causing plasma leakage. Thrombocytopenia results from immune complex deposition and bone marrow suppression, not direct platelet lysis alone.

Reference: Park's Textbook of Preventive and Social Medicine, 27th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.