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Cpx (4 each), and clades A, F, CRF01_AE and CRF36_cpx (2 each). In addition, 22 of the studied viruses apparently had nef and gag genes from viruses belonging to different clades, with the majority (8/10) having either a nef or gag gene derived from CRF02_AG. Interestingly, five gag sequences (10 ) and three (5 ) nef sequences were neither obviously recombinant nor easily classifiable into any
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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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Cpx (4 each), and clades A, F, CRF01_AE and CRF36_cpx (2 each). In addition, 22 of the studied viruses apparently had nef and gag genes from viruses belonging to different clades, with the majority (8/10) having either a nef or gag gene derived from CRF02_AG. Interestingly, five gag sequences (10 ) and three (5 ) nef sequences were neither obviously recombinant nor easily classifiable into any
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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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S clustered within the CRF02_AG clade, reinforcing the notion that this viral clade is a major contributor of genetic material to new recombinants [20]; an alternative explanation, however, could be that the gag and nef genes were amplified from different viruses co-infecting the same patients. Ongoing molecular and clinical surveillance will reveal whether new recombinants will begin to circulate
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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
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Les 1, 2). The sequences clustered with different clades and circulating recombinant forms distributed throughout the phylogenetic trees (Table 2), consistent with the breadth of HIV-1 diversity previously described in Cameroon. CRF02_AG-like viruses dominated the clade distribution, infecting 50 of the 46 participants for which both genes were sequenced (Figure 2). Participants infected with vir
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Mpled sequences are likely CRF02_AG (accounting for 50 of HIV-1M infections), with the other "pure" subtypes (G, D, A, and F) and CRFs (CRF11_cpx, 36_cpx, 37_cpx, and CRF01_AE) accounting for the remainder of infections. CRF02_AG and clade G viruses are broadly distributed across west central Africa and have apparently been circulating stably there for many years [3,17-19], consistent with the pr