42 research outputs found

    ESAT-6 and CFP-10- induced cytokine response in FluoroSpot.

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    <p>ESAT-6 induced cytokine immune response in 200.000 PBMCs/well in participants with active tuberculosis (TB, circle, n = 18), past tuberculosis (past TB, inverted triangle, n = 10), latent infection with <i>M</i>. <i>tuberculosis</i> (LTBI, square, ESAT-6-induced n = 24, CFP-10-induced n = 22), EliSpot-negative individuals (control, triangle, ESAT-6-induced n = 17, CFP-10-induced n = 19) was analysed. Groups had been defined according to the combination of their ESAT-6 and CFP-10 induced IFN-γ EliSpot-IGRA test result and clinical data. The number of IL-2<sup>+</sup> (A), INF-γ<sup>+</sup> (B), IL-2<sup>+</sup> INF-γ<sup>-</sup> (C), IL-2<sup>-</sup> INF-γ<sup>+</sup> (D) and IL-2<sup>+</sup> INF-γ<sup>+</sup> (E) spot-forming cells (SFC) were enumerated by FluoroSpot. (F) Mean proportion of ESAT-6 (top row) and CFP-10 (bottom row) -specific cytokine secreting cells for individuals with tuberculosis, past tuberculosis and LTBI are depicted as pie charts (light grey = IL-2<sup>+</sup> INF-γ<sup>-</sup>, black = IL-2<sup>-</sup> INF-γ<sup>+</sup> and dark grey = IL-2<sup>+</sup> INF-γ<sup>+</sup> secreting cells). Mann-Whitney U-test for non-parametric data was used for comparative analysis. A p-value of <0.05 was considered significant.</p

    Flow chart of patients included in this study.

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    <p>TB = tuberculosis; LTBI = latent infection with <i>M</i>. <i>tuberculosis;</i> control = healthy individual with negative EliSpot-IGRA result; E = ESAT-6; C = CFP-10; dark grey = positive test result in the EliSpot-IGRA; light grey = negative test result in the EliSpot-IGRA.</p

    Demographic characteristics of study subjects by groups.

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    <p>TB = tuberculosis.</p><p>LTBI = latent infection with <i>M</i>. <i>tuberculosis</i>.</p><p>m = male.</p><p>f = female.</p><p>n = number of cases.</p><p>Demographic characteristics of study subjects by groups.</p

    Detection of INF-γ<sup>+</sup> in EliSpot-IGRA and their concordance with INF-γ<sup>+</sup> results in FluoroSpot.

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    <p>ESAT-6 (A) and CFP-10 (B) -induced INF-γ<sup>+</sup> immune response in 200.000 PBMCs/well in participants with active tuberculosis (TB, circle, n = 18), past tuberculosis (past TB, inverted triangle, n = 10), latent infection with M. tuberculosis (LTBI, square, ESAT-6-induced n = 24, CFP-10-induced = 22) and EliSpot-negative individuals (control, triangle, ESAT-6-induced n = 17, CFP-10-induced n = 19) was analysed. LTBI and controls had been defined according to their ESAT-6 and CFP-10-induced IFN-γ EliSpot-IGRA test result and clinical data. Number of INF-γ<sup>+</sup> spot-forming cells (SFC) was enumerated by EliSpot. ESAT-6 (C) and CFP-10 (D) induced- INF-γ<sup>+</sup> SFC in EliSpot-IGRA (solid symbols) and FluoroSpot (open symbols) were analysed as matched pairs (connected with lines), differences were calculated using Wilcoxon signed rank test. Correlation between the number of ESAT-6 (E) and CFP-10 (F) specific INF-γ<sup>+</sup> spot-forming cells (SFC) in PBMC of 69 donors detected by FluoroSpot and EliSpot-IGRA. Concordance between EliSpot-IGRA and FluoroSpot results were assessed using R<sup>2</sup> coefficient. Agreement by Bland–Altman test was expressed as mean difference (horizontal solid line) and 95% limits of agreement (dashed line) between ESAT-6 (G) and CFP-10 (H) induced- INF-γ<sup>+</sup> SFC in FluoroSpot compared to EliSpot-IGRA.</p

    Cumulative incidence of grade 4–5 SAEs under 6 months BPaLM and standard of care.

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    The mean cumulative incidence of grade 4–5 SAEs ever experienced to each of 12 anti-TB drugs is shown for Strategy (1) (6 months BPaLM, DST upfront, repeat DST every 4 months, BPaLC if Mfx stopped) as compared to Strategy (7) (standard of care 9- to 18-month regimens based on results of upfront DST, repeat DST every 4 months). Estimates are provided per individual, averaged over the entire cohort initiating treatment. The mean estimate is shown by the bar, with 95% UIs represented as error bars. BPaLM, bedaquiline, pretomanid, linezolid, moxifloxacin; SAE, grade 4–5 severe adverse event; TB, tuberculosis; UI, uncertainty interval.</p

    Cohort prevalence of <i>M. tb</i>. resistance to key drugs at treatment initiation.

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    The proportion of the cohort with primary resistance to each drug is plotted, as described by M. tuberculosis whole genomic sequencing data from Moldova [30,35]. All those observations with rifampicin susceptibility were excluded, as per S2 Fig. *There was no resistance data for pretomanid; resistance was assumed to be at the same level as for delamanid. (PDF)</p

    Markov state-transition diagram.

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    Transitions between states can occur as shown by the arrows. Though not receiving treatment, individuals in the “Active TB, no longer receiving treatment” state are subject to a low rate of self-cure, and so may still transition to the “Cured post-treatment” state. Asterisks (*) highlight the major mechanisms through which the choice of treatment intervention affects outcomes. LTFU, lost to follow-up; TB, tuberculosis. Images within this figure were obtained as icons from Microsoft with no license or terms of use: https://support.microsoft.com/en-us/office/insert-icons-in-microsoft-365-e2459f17-3996-4795-996e-b9a13486fa79?ui=en-us&rs=en-us&ad=us. (PDF)</p

    Life years achieved under each RR-TB treatment strategy.

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    BPaL, bedaquiline, pretomanid, linezolid; BPaLC, bedaquiline, pretomanid, linezolid, clofazimine; BPaLM, bedaquiline, pretomanid, linezolid, moxifloxacin; UI, uncertainty interval. Strategies are listed in the same order as Table 3. Mean values are shown with accompanying 95% UIs in parentheses. (PDF)</p
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