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Ntegrin) (CD209) on dendritic cells [17-19]. Dendritic cells are considered crucial to fighting viral infections because of their ability to acquire and display viral antigens that would otherwisePage 2 of(page number not for citation purposes)Virology Journal 2009, 6:http://www.virologyj.com/content/6/1/evade the immune system. Dendritic cells affect the dengue virus in two ways. Immature dendrit
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Combine to form a C5 convertase. Runaway complement activation is prevented by binding of Complement Receptor 1 (CR1) and a constitutively active membrane bound Decay Accelerating Factor (DAF, or CD55) which can prevent the complement cascade[51]. In patients with severe dengue, large amounts of C3a have been detected revealing a role for complement in dengue pathogenesis. This finding might be an
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Orrespondence: Darrin.Martin@uct.ac.za; Wendy.Burgers@uct.ac.za 3 Computational Biology Group, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa 1 Division of Medical Virology, University of Cape Town, Cape Town, South Africain west central Africa, at 5.3 [8]. This, together with the co-circulation of divergent variants of multiple clades, h
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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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Duced CD55 promotes T-cell proliferation and Th1 cytokine expression. In addition to C3 production, APCs cleave C3 leading to autocrine and paracrine C3R signaling. C3R signaling promotes MHC class II expression, IL-12 production and B7 co-stimulatory molecules. Dendritic cells that fail to express C3aR suffer reduced T-cell activation. Anaphylatoxins are well known initiators of inflammation but