Abstract

DENGUE is an acute viral illness caused by the RNA virus of the family Flaviviridae and spread by Aedes mosquitoes. Intense dengue is a spreading cause of serious disease and death in some ’Asian and south American’ countries. Pathogenesis is associated with amended functioning of our innate immune system during infection. Toll Like Receptor is influential for the involucre of innate immunity able to cause of Dengue infection disease like pattern receptor recognition. Toll like receptor induces by injuries of a certain severity arbitrate activation of interferons and Fc receptor arbitrate involucre of cytokines. Clearance of Dengue virus is associated with interferons protein however regulatory mechanisms have been adopted against this modified effect. The clearance considers being a steady state known to be characterized low threshold level of DENV. The pathogenic state is characterized by high threshold level of SOCS. SOCS protein is also induced due to the interferon and cytokine amended signaling which can subsequently play its part in the regulation of interferon and cytokine production. Our hypothesis in this research the innate immunity system is associated between the pathogenesis of Dengue virus and the SOCS amended inhibition. We used the static formalism model of the biological regulatory network of Toll-like receptor induced by the pathogenesis of dengue amended signaling pathway. A model verification method used in GINsim was used to deduce the logical parameters for the qualitative modelling. Therefore, a multidisciplinary and translational study, constructed a formal model constraints approach with a static and integrative computational analysis, which may identify new immunopathological mechanisms and biomarkers for differential diagnosis, opening the way for the development of specific therapies that will reduce mortality and induced morbidity by Dengue virus.

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