Dengue induces platelet activation, mitochondrial dysfunction and cell death through mechanisms that involve DC‐SIGN and caspases

• Published in: Journal of thrombosis and haemostasis Vol. 11; no. 5; pp. 951 - 962
• Main Authors: Hottz, E. D., Oliveira, M. F., Nunes, P. C. G., Nogueira, R. M. R., Valls‐de‐Souza, R., Da Poian, A. T., Weyrich, A. S., Zimmerman, G. A., Bozza, P. T., Bozza, F. A.
• Format: Journal Article
• Language: English
• Published: England Elsevier Limited 01.05.2013
• Subjects: Adult; Apoptosis; Arbovirus; Case-Control Studies; Caspases - physiology; Cell Adhesion Molecules - physiology; Cell Death - physiology; DC‐SIGN; dengue; Dengue Virus - physiology; Drug therapy; Female; Humans; Lectins, C-Type - physiology; Male; Middle Aged; Mitochondria - physiology; mitochondrial dysfunction; platelet activation; Platelet Activation - physiology; Receptors, Cell Surface - physiology; thrombocytopenia

Summary Background Worldwide, dengue is the most prevalent human arbovirus disease. Dengue infection may cause a range of clinical manifestations from self‐limiting febrile illness through to a life‐threatening syndrome accompanied by both bleeding and shock. Thrombocytopenia is frequently observed...