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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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Helial cells, smooth muscles cells, and activated T-cells, but, interestingly, not na e T-cells. C5aR also activates a number of downstream signaling pathways including PI3K- (Phosophoinosital -3 Kinase), PLC (Phospholipase C), PLD (Phospholipase D), Raf and WASP (Wiskott-Aldrich syndrome protein). As a key modulator of the immune system, complement derived proteins clearly have the capacity to af
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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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Helial cells, smooth muscles cells, and activated T-cells, but, interestingly, not na e T-cells. C5aR also activates a number of downstream signaling pathways including PI3K- (Phosophoinosital -3 Kinase), PLC (Phospholipase C), PLD (Phospholipase D), Raf and WASP (Wiskott-Aldrich syndrome protein). As a key modulator of the immune system, complement derived proteins clearly have the capacity to af
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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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Reactive antibodies activate complement still further. The increase in alternative complement proteins, complement receptors and C protein all facilitate a positive feedback loop that can have dangerous consequences in a dengue infected patient.ConclusionThree immune components interact to produce a confluence of symptoms that define DHF/DSS. Dengue virus initially infects immature dendritic cells