Platelets were mainly associated with coagulation and hemostasis; however, other biological effects have been attributed to platelets, including angiogenesis, extracellular matrix synthesis, inflammation, and immune response. Dengue virus infection causes 200 million cases of severe flu-like illness annually, escalating to life-threatening hemorrhagic fever or shock syndrome. Some hypotheses are postulated for immunopathogenesis of dengue, including antibody enhancement theory, T-cell activation of cross-reactive memory, and original antigenic sin. All hypotheses, to some extent, induce an overproduction or a skewed profile of cytokine release, giving rise to the term cytokine storm/cytokine tsunami. Although thrombocytopenia is typical of both mild and severe diseases, the mechanism triggering platelet reduction is incompletely understood. In dengue, platelets are one of the major cell populations affected by direct and/or indirect mechanisms of infection. It is common to observe both thrombocytopenia and platelet dysfunction in dengue, both strongly related to the clinical outcome. Thus, platelets are frequently affected in dengue, either for alteration of their own functionality, for “silent transport” of virus, or as an anti-viral immune cell. In this way, we describe some of functional aspects of platelets on dengue, observing circulating mediators, intraplatelet proteins contents, morphology, activation markers, and ability to interact with dengue virus.
Part of the book: Thrombocytopenia