HIV-1 sequence evolution in vivo after superinfection with three viral strains-6

<p><b>Copyright information:</b></p><p>Taken from "HIV-1 sequence evolution in vivo after superinfection with three viral strains"</p><p>http://www.retrovirology.com/content/4/1/59</p><p>Retrovirology 2007;4():59-59.</p><p>Published online 23 Aug 2007</p><p>PMCID:PMC2020475.</p><p></p>tection of HIV-1 subtypes B (strains 1 and 2) and CRF01_AE in seminal plasma

HIV-1 sequence evolution in vivo after superinfection with three viral strains-1

<p><b>Copyright information:</b></p><p>Taken from "HIV-1 sequence evolution in vivo after superinfection with three viral strains"</p><p>http://www.retrovirology.com/content/4/1/59</p><p>Retrovirology 2007;4():59-59.</p><p>Published online 23 Aug 2007</p><p>PMCID:PMC2020475.</p><p></p>ormed on sequential blood plasma samples of patient H01-10366. The plasma viral loads measured by real-time, strain specific PCR is shown, as well as the overall plasma viral load determined with the VERSANT HIV-1 RNA 3.0 assay, which is based upon the gene. CD4+ cell counts (× 10) measured at the same time points are also shown

HIV-1 sequence evolution in vivo after superinfection with three viral strains-5

<p><b>Copyright information:</b></p><p>Taken from "HIV-1 sequence evolution in vivo after superinfection with three viral strains"</p><p>http://www.retrovirology.com/content/4/1/59</p><p>Retrovirology 2007;4():59-59.</p><p>Published online 23 Aug 2007</p><p>PMCID:PMC2020475.</p><p></p>anning position -147 to +67 of reference strain B (LAI) is shown at the top. Dashes indicate nucleotides that are identical in subtype B(LAI), gaps are represented by dots. Restriction sites used in cloning are italicised and underlined. Boxes indicate motifs possibly involved in promoter function [28]. Subtype AE has three unique transcription factor binding sites: an AP1 motif, a GABP motif and a CACCC box-binding factor motif [46,47]. The TAR hairpin sequence (position 176–232) is underlined. . Structure of the TAR RNA secondary structure in different HIV-1 subtypes, using the structure of subtypes B(LAI) and X [29] as references. Nucleotide differences between the strains are boxed and nucleotide deletions are indicated by (black triangle). A detailed phylogenetic analysis of HIV-1 subtype B TAR sequences has been described previously [48,49]. . Transcriptional activity of the HIV-1 LTR promoter sequences from strains B(LAI), X, B1, B2_S, B2_L, and AE. Transcriptional activity was tested in the presence of increasing concentrations of Tat. The value is the average of four independent measurements; the standard deviation is indicated

HIV-1 sequence evolution in vivo after superinfection with three viral strains-7

<p><b>Copyright information:</b></p><p>Taken from "HIV-1 sequence evolution in vivo after superinfection with three viral strains"</p><p>http://www.retrovirology.com/content/4/1/59</p><p>Retrovirology 2007;4():59-59.</p><p>Published online 23 Aug 2007</p><p>PMCID:PMC2020475.</p><p></p>ormed on sequential blood plasma samples of patient H01-10366. The plasma viral loads measured by real-time, strain specific PCR is shown, as well as the overall plasma viral load determined with the VERSANT HIV-1 RNA 3.0 assay, which is based upon the gene. CD4+ cell counts (× 10) measured at the same time points are also shown

HIV-1 sequence evolution in vivo after superinfection with three viral strains-0

<p><b>Copyright information:</b></p><p>Taken from "HIV-1 sequence evolution in vivo after superinfection with three viral strains"</p><p>http://www.retrovirology.com/content/4/1/59</p><p>Retrovirology 2007;4():59-59.</p><p>Published online 23 Aug 2007</p><p>PMCID:PMC2020475.</p><p></p>tection of HIV-1 subtypes B (strains 1 and 2) and CRF01_AE in seminal plasma

HIV-1 sequence evolution in vivo after superinfection with three viral strains-3

<p><b>Copyright information:</b></p><p>Taken from "HIV-1 sequence evolution in vivo after superinfection with three viral strains"</p><p>http://www.retrovirology.com/content/4/1/59</p><p>Retrovirology 2007;4():59-59.</p><p>Published online 23 Aug 2007</p><p>PMCID:PMC2020475.</p><p></p>llected in 2001–2005. Distances were calculated with the Tamura-Nei method using the gamma model with α = 0.25, and 1000 bootstrap replicated were analysed. The three separate clusters comprised of strains B1, B2, and CRF01_AE are indicated. A representative sequence set was used to draw the phylogenetic tree

Additional file 1: Table S1. of Widespread hepatitis B virus genotype G (HBV-G) infection during the early years of the HIV epidemic in the Netherlands among men who have sex with men

Contains the sequences of the PCR-primers used in the study. (XLS 39 kb

Additional file 1: Table S1. of Widespread hepatitis B virus genotype G (HBV-G) infection during the early years of the HIV epidemic in the Netherlands among men who have sex with men

Contains the sequences of the PCR-primers used in the study. (XLS 39 kb

Percentage of cells expressing CD14, CD16, and/or sialoadhesin of the total PBMC fraction, as determined by FACS analysis

<p>Percentage of cells expressing CD14, CD16, and/or sialoadhesin of the total PBMC fraction, as determined by FACS analysis</p

Expression of CD14, CD16, and sialoadhesin on monocytes from an HIV-1 infected and uninfected patient.

<p>A. Sialoadhesin (CD169) expression on CD14⁺ cells from a healthy human control (left) and an HIV-1 infected patient (right). The mean fluorescent intensity of CD169 from the CD14⁺ cells increases from 26 in the control cells (left) to 286 in the cells from the HIV-1 infected patient (right). B. CD14⁺CD16⁺ cells were gated and their expression of sialoadhesin is shown in the histograms. The mean fluorescent intensity of CD169 from the CD14⁺CD16⁺ cells increases from 17 in the control cells (left) to 158 in the cells from the HIV-1 infected patient (right). The data are representative of three experiments.</p