Dengue-2 interactions with complement and coagulation cascades (WP3896)

Dengue virus infection can give rise to hemorrhagic shock. Highlighted in red are Dengue-2 structural protein interactions with human proteins involved in coagulation, building upon the complement and coagulation cascades described in http://wikipathways.org/index.php/Pathway:WP558 by the following text: Blood coagulation is a series of coordinated and calcium-dependent proenzyme-to-serine protease conversions likely to be localized on the surfaces of activated cells in vivo. It culminates in the formation of thrombin, the enzyme responsible for the conversion of soluble fibrinogen to the insoluble fibrin clot. The kallikrein-kinin system is an endogenous metabolic cascade, triggering of which results in the release of vasoactive kinins (bradykinin-related peptides). Kinin peptides are implicated in many physiological and pathological processes including the regulation of blood pressure and sodium homeostasis, inflammatory processes, and the cardioprotective effects of preconditioning. Complement is a system of plasma proteins that is activated by the presence of pathogens. There are three pathways of complement activation: the classical pathway, the lectin pathway, and the alternative pathway. All of these pathways generate a crucial enzymatic activity that, intern, generates the effector molecules of complement. The three main consequences of complement activation are the opsonization of pathogens, the recruitment of inflammatory and immunocompetent cells, and the direct killing of pathogens. Source: KEGG (http://www.genome.jp/dbget-bin/www_bget?pathway:map04610)

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