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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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Hose residing on isolated branches outside of subtrees containing previously defined HIV-1 subtype or CRF lineages. Outlier sequences on the other hand were defined as those residing on basal branches of subtrees containing previously defined HIV-1 subtype or CRF lineages. Nucleotide sequences were deposited in GenBank [JX244899-JX244948 for gag and JX244949JX245003 for nef]. Clinical and demograp
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Ibution of HIV-1 in CameroonSample ID BS01 BS02 BS03 BS04 BS05 BS06 BS09 BS10 BS11 BS12 BS13 BS14 BS16 BS18 BS19 BS20 BS21 BS22 BS23 BS24 BS25 BS26 BS27 BS29 BS30 BS31 BS32 BS35 BS38 BS39 BS40 BS42 BS43 BS44 BS45 BS46 BS47 BS48 BS49 BS50 BS51 BS53 BS54 BS55 gag gene CRF02_AG A-like G G CRF02_AG CRF02_AG CRF02_AG A1 CRF02_AG G CRF02_AG CRF02_AG CRF02_AG NDc CRF02_AG NDc CRF02_AG CRF02_AG CRF02_AG C
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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