Comparison of the transcriptional profiles of patients with dengue fever and dengue hemorrhagic fever reveals differences in the immune response and clues in immunopathogenesis.

摘要: Introduction. Dengue infection demonstrates a wide spectrum of clinical manifestations from mild disease (dengue fever) to severe dengue hemorrhagic fever, but the immunopathogenic mechanisms involved in severity are not clear. Objective. Differentially expressed genes associated immune response were indentified peripheral blood mononuclear cells Colombian children with fever and fever. Materials methods. Microarray analysis was used as tool establish compare transcriptional profiles six acute phase The commercial gene chip Affymnetrix GeneChip HG_U133_Plus_2. Results. patients interleukin 6, chemokines, complement proteins pentraxin 3, along lymphocyte inhibitors lymphocyte-activation 3 cathepsin L1. An interaction model for these showed tissue factor playing central role network generated. In contrast, cytokines, leukotrienes lactotransferrin, C1 inhibitor, leukotriene-B (4-omega-hydroxylase 2). Conclusions. These results indicate that cytokine able limit endothelial damage prevent increases vascular permeability, whereas dengue-hemorrhagic have cell dysfunction unregulated action. This leads "hypercoagulation" damage, thereby increasing severity. Verification pathogenic identified molecules will contribute understanding pathogenesis lead rational development therapeutic drugs.