15 research outputs found

    Functional activities against HIV-1 of immunoglobulins purified from pooled stool samples of children breastfed by HIV-1-infected milk.

    No full text
    <p>Immunoglobulins (Ig) purified by immunoaffinity from pooled stool samples from 8 HIV-1-infected mothers and their breast milk exposed non HIV-infected babies (group I) and 6 couples of HIV-1-infected mothers and their breastfed HIV-1-infected babies (group II), and containing F(ab’)2 to gp160 with similar specific activities, were constituted. <b>A and B.</b> Inhibition of the attachment of HIV-1NDKon HT29 cells and of HIV-1NDKand HIV-1JRCSF on monocyte-derived macrophages (MDM) by Ig purified from pooled stools of children breastfed by HIV-1-infected milk.HT29 intestinal cell lines and MDM were incubated with HIV-1NDKor HIV-1JRCSFin the presence of 30 (A) or 50 (B) µg/ml of pooled stools purified Igfor 1 hour at 37°C. Cells were then washed, lysed, and quantities of attached virus were evaluated by HIV p24 antigen measurement in the culture lysate using capture ELISA. Lactoferrin and the monoclonal antibody IgG1B12 were used as positive controls for inhibition; IVIg and total Ig purified from pooled stools of HIV non exposed, HIV-seronegative babies were used as negative controls. The experiments were carried out in triplicate with cells from three different donors. The HIV-1NDK or HIV-1JRCSF attachment inhibitions are expressed as percentage ± standard error of three independent experiments; <b>C.</b> Inhibition of the HIV-1JRCSF infection of MDM by Ig (50 µg/ml) purified from pooled stools of children breastfed by HIV-1-infected milk.The monoclonal antibody IgG2G12 was used as positive control for inhibition; IVIg and total Ig purified from pooled stools of HIV non exposed, HIV-seronegative babies were used as negative controls. The levels of viral production at day 6 postinfection were assessed by HIV p24 antigen measurement in the culture supernatants using capture ELISA. The experiments were carried out in triplicate with cells from three different donors. The HIV-1JRCSF infection inhibition is expressed as percentage ± standard error of three independent experiments. <i>Nota bene</i>. HT-29 epithelial cells were stained with mouse phycoerythrin (PE)-conjugated monoclonal antibodies anti-CD4 (Leu3a) (Becton Dickinson Biosciences, Mountain View, CA) and CXCR4 (12G5) (BD PharMingen, Le Pont de Claix, France), and with fluorescein isothiocyanate (FITC)-conjugated anti-human monoclonal antibodies DC-SIGN (DCN46) and CCR5 (2D7) from BD Biosciences (San Diego, CA) and GalCer (MAB342) (Chemicon International, Paris, France). Analysis was assessed using a FACSCalibur flow cytometer and CellQuest software (BD Biosciences). Results are presented as the percentage of receptor-positive cells. Forty-six percent of HT-29 cells expressed GalCer, 29% CXCR4 and 10% CCR5, whereas very low (<0.1%) expression of CD4 and DC-SIGN was detected.</p

    Main characteristics of study mother-child couples, including 8 couples of HIV-1-infected mothers and their breastfed non HIV-infected babies (group I), and 6 couples of HIV-1-infected mothers and their breastfed HIV-1-infected babies (group II).

    No full text
    ÂŁ<p>World Health Organization (WHO) clinical staging of HIV/AIDS for adults and adolescent with established HIV infection according to the 2010-revised WHO recommendations for HIV care in in babies and children for resource-limited settings <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0063408#pone.0063408-WHO2" target="_blank">[31]</a>;</p>$<p>WHO clinical staging of HIV/AIDS for children with established HIV infection according to the 2010-revised WHO recommendations for HIV care in babies and children for resource-limited settings <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0063408#pone.0063408-WHO1" target="_blank">[30]</a>; CD4 T cell count in infants were not available because the national AIDS programme has focused on universal treatment for infants less than 12 months, independently of their clinical or immunological status;</p>*<p>Plasma HIV-1 RNA load was measuredby the Generic HIV-1 RNA quantification assay (Biocentric, Bandol, France), which threshold of detectability is 300 copies/ml <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0063408#pone.0063408-Rouet2" target="_blank">[35]</a>.The molecular diagnosis of HIV infection was carried out at time of sampling; the timing of HIV infection in study children could not be assessed.</p><p>NA: Not applicable.</p

    Levels of total IgA, IgG and IgM in breast milk (white bars in left) and children’s stools (black bars in right) samples from 8 HIV-1-infected mothers and their breast milk exposed non HIV-infected babies (group I), 6 couples of HIV-1-infected mothers and their breastfed HIV-infected babies (group II), and 10 healthy HIV-negative breast-feeding women and their breastfed non HIV-infected babies as negative controls.

    No full text
    <p>The mean concentrations of milk IgA were higher than those of IgG or IgM in HIV-infected mothers as in HIV-negative mothers. The levels of milk IgG was 5.5 higher in HIV-infected mothers than in HIV-negative mothers. The levels of stool IgA and IgG in babies born from HIV-infected mothers were higher than those of HIV-negative control babies. Immunoglobulins levels are expressed in µg/ml ± standard error. The stars indicate the significant differences by comparison to HIV-negative control samples (* P<0.01).</p

    Pathogen load in different age categories.

    No full text
    <p><b>A:</b> Pathogen load by age category for the three main groups of pathogens, parasites (white bars), bacteria (grey bars) and viruses (black bars). <b>B</b>: Infection with multiple pathogens by age category. White bars indicate the presence of at least one pathogen of any group (parasite, bacteria or virus), grey bars the presence of at least two pathogens of any group (parasite, bacteria or virus) and black bars indicate mixed infections with at least one representative of two different groups (virus, parasite or bacteria) in the same child. Infant: 0–11 months, Toddler: 12–23 months; Child: ≥ 24 months).</p

    Hepatitis B and hepatitis D virus infections in the Central African Republic, twenty-five years after a fulminant hepatitis outbreak, indicate continuing spread in asymptomatic young adults

    Get PDF
    <div><p>Hepatitis delta virus (HDV) increases morbidity in Hepatitis B virus (HBV)-infected patients. In the mid-eighties, an outbreak of HDV fulminant hepatitis (FH) in the Central African Republic (CAR) killed 88% of patients hospitalized in Bangui. We evaluated infections with HBV and HDV among students and pregnant women, 25 years after the fulminant hepatitis (FH) outbreak to determine (i) the prevalence of HBV and HDV infection in this population, (ii) the clinical risk factors for HBV and/or HDV infections, and (iii) to characterize and compare the strains from the FH outbreak in the 1980s to the 2010 HBV–HDV strains. We performed a cross sectional study with historical comparison on FH-stored samples (n = 179) from 159 patients and dried blood-spots from volunteer students and pregnant women groups (n = 2172). We analyzed risk factors potentially associated with HBV and HDV. Previous HBV infection (presence of anti-HBc) occurred in 345/1290 students (26.7%) and 186/870 pregnant women (21.4%)(<i>p = 0</i>.<i>005</i>), including 110 students (8.8%) and 71 pregnant women (8.2%), who were also HBsAg-positive (<i>p = 0</i>.<i>824</i>). HDV infection occurred more frequently in pregnant women (n = 13; 18.8%) than students (n = 6; 5.4%) (<i>p = 0</i>.<i>010</i>). Infection in childhood was probably the main HBV risk factor. The risk factors for HDV infection were age (<i>p = 0</i>.<i>040</i>), transfusion (<i>p = 0</i>.<i>039</i>), and a tendency for tattooing (<i>p = 0</i>.<i>055</i>) and absence of condom use (<i>p = 0</i>.<i>049</i>). HBV-E and HDV-1 were highly prevalent during both the FH outbreak and the 2010 screening project. For historical samples, due to storage conditions and despite several attempts, we could only obtain partial HDV amplification representing 25% of the full-length genome. The HDV-1 mid-eighties FH-strains did not form a specific clade and were affiliated to two different HDV-1 African subgenotypes, one of which also includes the 2010 HDV-1 strains. In the Central African Republic, these findings indicate a high prevalence of previous and current HBV-E and HDV-1 infections both in the mid-eighties fulminant hepatitis outbreak and among asymptomatic young adults in 2010, and reinforce the need for universal HBV vaccination and the prevention of HDV transmission among HBsAg-positive patients through blood or sexual routes.</p></div
    corecore