Abstract
Dengue hemorrhagic fever (DHF) is a serious public health problem. Increased vascular permeability and thrombocytopenia are the hallmarks of DHF. The mechanisms involved in DHF/Dengue shock syndrome (DSS) pathogenesis is not fully understood. This study gives evidence of the presence of antibodies which cross-reacted with platelets, and endothelial cells in the sera of Vietnamese infants and children with DHF/DSS. The anti-platelet, anti-endothelial cell IgM levels were higher in the sera of DHF/DSS infants and children, compared with controls. However, the levels of these autoantibodies were not correlated with the severity of DHF (non-shock DHF vs DSS). The antiplatelet, and anti-endothelial cell autoantibodies may play a role in the pathogenesis of DHF/DSS in infants and children with predominantly primary, and secondary dengue infections, respectively. The epitopes shared by surface molecules of platelets and endothelial cells and dengue virus antigens need to be identified and avoided in designing the safe candidate vaccines.
Highlights
Dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS) caused by dengue virus infection is a serious public health problem worldwide[1,2]
Patients: Fifty infants, ages less than 12 months, admitted to the Department of Dengue Hemorrhagic Fever, Children’s Hospital N.1- Ho Chi Minh City from May, 1998 to March, 2002, and 37 children, ages of 415 years, admitted from September to November, 2001 with clinical diagnosis of DHF/DSS according to the criteria of the World Health Organization[2] which were confirmed by positive viral envelope and membrane (E/M)-specific capture immunoglobulin M (IgM) and IgG enzyme-linked immunosorbent assays (ELISA) were enrolled in the study
We found that sera from 10 infants infected with DEN-3, and 4 with DEN-4 had anti-platelet IgM
Summary
Dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS) caused by dengue virus infection is a serious public health problem worldwide[1,2]. An estimated 50 million infections occur annually, including 500,000 cases of DHF/ DSS, at least 2.5% of cases die[3]. The immunopathogenesis of dengue virus infection with emphasis on the immune deviation, autoantibodies, and cytokine production has been proposed[6]. It is possible that capillary endothelial cells may mediate the vascular leakage. Dengue virus replicates readily in cultures of human endothelial cells[7,8,9], there is no evidence of necrosis of endothelial cells nor infiltration of inflammatory cells into blood vessel walls in human tissues studied at biopsy or autopsy[4,10]. The mechanism of the endothelial barrier disruption leading to plasma leakage in DHF/DSS is not fully known
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