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Ormation were obtained. RNA was extracted from plasma samples, reverse transcribed and PCR amplified as described previously [12] using subtype non-specific HIV-1 primers for HIV-1 full length gag [12] and nef [13] genes, and sequenced. Sequenced fragments were assembled using ChromasPro. Full length gag and nef sequences were generated and aligned using MUSCLE with manual editing in MEGA5, togeth
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Trees were constructed from these sequences with 100 full maximum likelihood bootstrap replicates (implemented in PHYML [14]), following either complete removal of recombinant sequence fragments or the division of recombinant sequences into their constituent fragments by a blinded fully exploratory screen for recombination using RDP3 [15]. The recombination screen was fully exploratory in that eve
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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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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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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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Two samples for which only gag or nef was typed, these were classified as belonging to CRF11_cpx. Notably, despite subtypes B and C collectively accounting for approximately 75 infections worldwide [16], none of our sequences were classified as belonging to either of these clades. In 10/46 samples from which both nef and gag sequences were analysed, they were classified as belonging to different
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Ceable by EGFR upstream directed therapeutic agents (i.e. cetuximab and panitumumab). Tumor NF-kB and B-RAF mutation status are interesting examples of such molecular factors [12,21]. However none of these factors seemed strong enough to translate into clinical practice, mostly because these response determinants singularly taken do not account of all responding (or resistant) patients. The presen
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Two samples for which only gag or nef was typed, these were classified as belonging to CRF11_cpx. Notably, despite subtypes B and C collectively accounting for approximately 75 infections worldwide [16], none of our sequences were classified as belonging to either of these clades. In 10/46 samples from which both nef and gag sequences were analysed, they were classified as belonging to different