From the Research
Dengue fever's pathophysiology involves a complex interplay of host immunity, genetic predisposition, and viral virulence factors, leading to immune-mediated responses and potential severe disease outcomes, as supported by recent studies 1. The pathophysiology of dengue fever is characterized by the infection of macrophages, dendritic cells, and monocytes by the dengue virus, which triggers an immune response, including the release of cytokines and chemokines that cause the characteristic fever, headache, and muscle pain.
- Key factors contributing to the pathogenesis of dengue include:
- Antibody-dependent enhancement, where pre-existing antibodies from previous dengue infections bind to the new virus but fail to neutralize it, instead facilitating increased viral entry into cells 2.
- The role of T-cell immunopathology, with cross-reactive high pro-inflammatory cytokine producing T cells predominating in severe dengue 3.
- The involvement of toll-like receptors and antiviral responses in the innate immune response to dengue virus 4.
- The impact of viral and host factors, such as NS1 protein and anti-DENV NS1 antibodies, on disease susceptibility and severity 5. In severe cases, the pathophysiology becomes more complex, leading to excessive immune activation, a cytokine storm, and potential progression to dengue hemorrhagic fever or dengue shock syndrome.
- The clinical manifestations of severe dengue include:
- Thrombocytopenia due to decreased platelet production and increased destruction.
- Liver involvement causing elevated transaminases and potential jaundice.
- Bone marrow suppression, reducing white blood cell counts. Treatment remains supportive, focusing on adequate hydration, fever management with acetaminophen, and close monitoring for warning signs of severe disease, as no specific antiviral therapy exists 1.