1
D increases permeability of small blood vessels and smooth muscle contraction. In macrophages, eosinophiles, and neutrophils anaphylatoxins can induce oxidative burst, basophiles, and mast cells release histamine, and C3a can enhance the effect of other proinflammatory cytokines such as TNF, IL-6, and SDF-1. While the mechanism for the many reactions precipitated by complement anaphylatoxins has n
1
Replicates following removal of recombinant sequence fragments by a blinded fully exploratory screen for recombination using RDP3. Black squares at the end of the branches represent the gag and nef sequences sampled from Cameroon in this study, while red squares represent intragene recombinant fragments in our samples. The gag tree was rooted using HIV-1 group N, O, P and SIV CPZ isolates, while t
1
Replicates following removal of recombinant sequence fragments by a blinded fully exploratory screen for recombination using RDP3. Black squares at the end of the branches represent the gag and nef sequences sampled from Cameroon in this study, while red squares represent intragene recombinant fragments in our samples. The gag tree was rooted using HIV-1 group N, O, P and SIV CPZ isolates, while t
1
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
1
D increases permeability of small blood vessels and smooth muscle contraction. In macrophages, eosinophiles, and neutrophils anaphylatoxins can induce oxidative burst, basophiles, and mast cells release histamine, and C3a can enhance the effect of other proinflammatory cytokines such as TNF, IL-6, and SDF-1. While the mechanism for the many reactions precipitated by complement anaphylatoxins has n
1
A CRF02_AGa CRF02_AGa CRF02_AGaCRF02_AG CRF22_01A1 CRF02_AG CRF02_AG CRF36_cpxb/F2b CRF02_AG NDc CRF02_AG CRF02_AG ND NDc cCRF02_AG CRF01_AE CRF02_AG CRF02_AG CRF01/F CRF02_AG A-likeb CRF02_AG CRF02_AG CRF01_AE CRF02_AG NDc CRF02_AGNDc CRF02_AG A1 A1 F G A1 CRF02_AG CRF02_AG CRF02_AG CRF02_AG CRF02_AG CRF02_AG CRF02_AG CRF02_AG CRF37_cpx F CRF01_AE CRF37_cpx Ub DCRF02_AGa CRF02_AG URF A1 URF G URF
1
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
1
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