78 research outputs found

    ‘Brown sugar’ heroin intoxication and improvement of surrogate immunologic markers in HIV infection

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    ObjectiveTo report on the unexpected improvement in major biological surrogate markers (CD4T-cell count, HIV RNA viral load, and apoptosis level) during the periods of ‘brown sugar’ heroin intoxication (BSD in 12 HIV-1-infected intravenous drug users, independently of their antiretroviral therapy, compared to the period of ‘brown sugar’ heroin withdrawal (BSW).MethodsThe patients were followed prospectively for a total of 417 months over 4 years. Twenty-four episodes of BSI and 24 periods of BSW were analyzed.Results(1) BSI: the mean (±SE) duration was 9±1.8 months; at onset, the mean±SE CD4T-cell count was 401±88/mm3; at the end, an absolute increase of 346 CD4T-cells/mm3 and a CD4T-cell count relative variation of + 131% was observed. Half of the patients showed an increase of CD4 T-cell count of more than 90% during their follow-up. The mean±SE of CD8 T-cell count increased significantly by 108%. (2) BSW: the mean ±SE duration was 8.4±1.3 months; at onset, the mean ±SE CD4 T-cell count was 695±78/mm3; at the end, an absolute decrease of 342 CD4 T-cells/mm3 and a CD4 T-cell count relative variation of −52% was observed. Half of the patients showed a decrease of CD4 T-cell count of more than 51%. (3) Circulating viral load appeared to be significantly higher during BSW (median: 452000 Eq RNA/mL) than during BSI (median: 52 000 Eq RNA/mL); p<O.01. (4) Similarly, the apoptotic process affecting circulating lymphocytes was significantly lower during BSI than during BSW episodes. (5) The 4-year mortality rate was 7%, compared with 36% in HIV-positive former drug users (p<0.001).ConclusionsTaken together, these features suggest that ‘brown sugar’ heroin could have either immunomodulatory or antiretroviral properties. Confirmation of these findings and investigation of the role of the many substances in ‘brown sugar’ heroin are indicated

    Post-treatment controllers differ from HIV controllers in terms of HLA class I profile, frequency and quality of the CD8+ T cell response and activation levels of CD8+ T cells.

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    <p><b>A.</b> The frequencies of the protective alleles HLA-B*27 and B*57 and the risk alleles HLA-B*07 and B*35 in the general French population (n = 6094 alleles <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1003211#ppat.1003211-Alizadeh1" target="_blank">[20]</a>, <a href="http://www.allelefrequencies.net" target="_blank">www.allelefrequencies.net</a>), HICs (n = 148 alleles) and PTCs (n = 28 alleles). The statistical analyses are shown in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1003211#ppat.1003211.s006" target="_blank">Table S2</a>. <b>B.</b> The frequency of HIV-specific CD8+ T cells, estimated as the number of CD8+ T cells producing IFN-γ upon stimulation with optimal HIV-1 peptides (spot-forming cells, SFC) in untreated viremic patients (VIRs) (n = 57), treated patients (ARTs) (n = 60), HICs (n = 100) and PTCs (n = 12). <b>C.</b> The capacity of CD8+ T cells from VIRs (n = 22), ARTs (n = 14), HICs (n = 73) and PTCs (n = 14) to suppress the HIV-1 infection of autologous CD4+ T cells, as determined by the log-fold decrease in the level of secreted p24 (CD4 vs. CD4∶CD8 1∶1 cell cultures). <b>D.</b> The percentage of CD8+ T cells from ARTs (n = 5), HICs (n = 58) and PTCs (n = 8) that expressed CD38, HLA-DR or both CD38 and HLA-DR ex vivo. <b>B, C and D.</b> The mean and standard deviation for each group are shown.</p
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