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Dengue is an infectious disease caused by dengue virus DENV. In general, dengue is a self-limiting acute febrile illness followed by a phase of critical defervescence, in which patients may improve or progress to a severe form. Severe illness is characterized by hemodynamic disturbances, increased vascular permeability, hypovolemia, hypotension, and shock.
Thrombocytopenia and platelet dysfunction are common in both cases and are related to the clinical outcome. Different mechanisms have been hypothesized to explain DENV-associated thrombocytopenia, including the suppression of bone marrow and the peripheral destruction of platelets.
Studies have shown DENV-infected hematopoietic progenitors or bone marrow stromal cells. It is not yet clear whether platelets play a role in the viral spread. Here, we focus on the mechanisms of thrombocytopenia and platelet dysfunction in DENV infection.
Finally, an implication for platelets in plasma leakage will be also regarded, as thrombocytopenia is associated with clinical outcome and higher mortality. Dengue causes serious infection in humans, resulting in morbidity and mortality in most tropical and subtropical areas of the world. The structural proteins include a capsid protein C that binds viral RNA [ 4 ], a Membrane protein M found in the mature viral particle, and an envelope E protein that mediates viral attachment, membrane fusion, and virion assembly [ 5 ].
