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Review
. 2009 Dec;102(6):1042-9.
doi: 10.1160/TH09-03-0208.

Plasma leakage in dengue haemorrhagic fever

Anon Srikiatkhachorn  1
Affiliations
Review

Plasma leakage in dengue haemorrhagic fever

Anon Srikiatkhachorn. Thromb Haemost. 2009 Dec.

Abstract

Dengue viruses (DENV), a group of four serologically distinct but related flaviviruses, are the cause of one of the most important emerging viral diseases. DENV infections result in a wide spectrum of clinical disease including dengue haemorrhagic fever (DHF), a viral haemorrhagic disease characterised by bleeding and plasma leakage. The characteristic feature of DHF is the transient period of plasma leakage and a haemorrhagic tendency. DHF occurs mostly during a secondary DENV infection. Serotype cross-reactive antibodies and mediators from serotype cross-reactive Dengue-specific T cells have been implicated in the pathogenesis. A complex interaction between virus, host immune response and endothelial cells likely impacts the barrier integrity and functions of endothelial cells leading to plasma leakage. Recently the role of angiogenic factors and the role of dengue virus on endothelial cell transcription and functions have been studied. Insights into the mechanisms that confer protection or cause disease are critical in the development of prophylactic and therapeutic modalities for this important disease.

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Figures

Figure 1
Figure 1. Clinical course of DF and DHF
An abrupt onset of high, persistent fever is an early manifestation of both DF and DHF. During the febrile phase, patients may develop other signs and symptoms including headache, myalgia and variable degrees of hemorrhagic tendency. Platelet counts decline during this stage, reaching the lowest point around the time of defervescence. During defervescence, some patients develop a transient increase in vascular permeability resulting in leakage of albumin rich fluid in the pleural and abdominal cavities. This is associated with hemoconcentration as indicated by an increase in hematocrit. Evidence of plasma leakage and thrombocytopenia (platelet count < 100,000/cumm) are the two criteria differentiating DHF from DF. The plasma leakage usually resolves after 48 hours followed by a convalescence period.
Figure 2
Figure 2. Immunopathogenesis of DHF
Primary exposure to dengue virus induces both humoral (antibodies) and cellular (T cells) mediated immune responses. During a secondary infection with a different dengue virus serotype, cross-reactive, non-neutralizing antibodies bind to virus and enhance viral uptake via Fc receptors resulting in enhanced viral replication and higher antigen load which lead to an exaggerated activation of cross-reactive dengue specific T cells. Dengue virus may have direct effects on endothelial cell such as modulation of cell surface molecule and cytokine receptor expression. Biological mediators released by T cells and by virus infected cells along with complement activation by viral proteins and immune complexes, may result in enhanced vascular permeability and coagulopathy.
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