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Hway begins with the formation of an antibody C1q complex on the surface of a pathogen or pathogen infected cell. This complex, in turn, activates C2 via serine proteases and is itself also a serine protease[49]. The protein C2a combines with newly cleaved protein C4a to generate a C3 convertase, C2aC4b. C3b forms the central protein complex of the complement system either by binding to complement
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Om neutrophils, eosinophiles, and basophiles. C3a and C5a act on specific receptors to produce local inflammatory responses and when secreted in concentrations high enough to invoke a general systemic response, they cause circulatory collapse similar to an IgE mediated allergic response. ATs modulate the secretion of IL-6, and TNF from B cells and serve as potent chemoattractants[52]. C5a also wor
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Neutralization. However, in heterotypic dengue virus infections the antibodies are non-neutralizing and lead to enhancement. Two cell lines expressing either FcRIA or FcRIIA have been used to demonstrate that immune complexes can enhance virus infectivity in an FcR mediated fashion. FcRIA is found exclusively on macrophages and dendritic cells and preferentially binds monomeric IgG, while FcRIIA i
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Use tissues[47]. There is a high correlation between NS1 concentration in patient sera and high concentrations of anaphylatoxins which suggests a role for NS1 in complement activation. Further, anaphylatoxins are co-localized to the lungs and plasma in dengue infections. Co-localization experiments with membrane bound NS1 and NS1 specific antibodies showed the formation of complement attack comple
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Ells can increase viral RNA production by over 100-fold making dendritic cells potent components in dengue pathogenesis[20]. Infected dendritic cells also contribute to vascular leak through the production of matrix metalloproteinases (MMPs). MMP-2, MMP-13, and MMP-9 were all dramatically increased in immature dendritic cells infected with DENV2. As a result cell-cell adhesion in cells co-cultured
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Anti-NS1 antibodies stimulating the release of IL-6, IL-8, and MCP-1 in an NFB-dependent manner. Correlated with antibody binding is the upregulation of ICAM1. ICAM1 upregulation can facilitate the adherence of PBMCs to the endothelium. Both NFB inhibitors and soluble NS1 to block the antiNS1 antibodies can able to block cytokine release in vitro[46]. Using ELISA flow cytometry, it can be shown th
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Neutralization. However, in heterotypic dengue virus infections the antibodies are non-neutralizing and lead to enhancement. Two cell lines expressing either FcRIA or FcRIIA have been used to demonstrate that immune complexes can enhance virus infectivity in an FcR mediated fashion. FcRIA is found exclusively on macrophages and dendritic cells and preferentially binds monomeric IgG, while FcRIIA i
1
Ivation is greatly enhanced. When they added purified NS1 protein to normal or convalescent sera they found synonymous results with NS1 activating complement and complement activation being synergized by anti-dengue antibodies. While NS1 could clearly activate complement in the fluid phase it was unable activate complement when stably expressed on the surface of cells. However, when patient sample

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