14 research outputs found

    CMV-specific T cell responses in HIV uninfected and infected adults.

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    <p>NOTE. Median values and interquartile ranges are shown. All subjects contributed pp65-specific IFN-γ-bright data (n = 685), while only a subset contributed pp65 and IE data (see text). IE data were not available from the recently infected subjects. The combined pp65 and IE interferon-γ/IL2 data reflect the sum of all possible response (IFN-γ alone, IL2 alone and IFN-γ/IL2) to each of the CMV protein.</p

    The distribution of the CMV-specific CD4+ and CD8+ T cell responses (background corrected) in three unique groups: (1) HIV-seronegative, CMV-seropositive, (2) established chronic untreated HIV infection, and (3) antiretroviral-treated infection with undetectable plasma HIV RNA levels.

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    <p>The IE IFN-γ-bright levels are shown in panel A (CD4+ T cells) and panel B (CD8+ T cells). The combined pp65 and IE IFN-γ/IL2 data are shown in panels C (CD4+ T cells) and panel D (CD8+ T cells). The data in panels C and D reflect the sum of all possible response (IFN-γ alone, IL2 alone, or IFN-γ/IL2) to each of the CMV proteins. Standard gating was used for dual cytokine data.</p

    The distribution of pp65 IFN-γ-bright CD4+ and CD8+ T cell responses (background corrected) in four unique groups: (1) HIV-seronegative, CMV-seropositive, (2) acute and recent untreated HIV infection, (3) established chronic untreated HIV infection, and (4) antiretroviral-treated infection with undetectable plasma HIV RNA levels.

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    <p>The distribution of pp65 IFN-γ-bright CD4+ and CD8+ T cell responses (background corrected) in four unique groups: (1) HIV-seronegative, CMV-seropositive, (2) acute and recent untreated HIV infection, (3) established chronic untreated HIV infection, and (4) antiretroviral-treated infection with undetectable plasma HIV RNA levels.</p

    Patient characteristics.

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    a<p>HAART initiated during acute/early or chronic HIV-1 infection as defined in <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1003174#s4" target="_blank">Methods</a>.</p>b<p>W, white, non-Hispanic; H, Hispanic; AA, African-American; As, Asian; M, mixed race.</p>c<p>Time after infection before achieving the most proximally documented period of sustained suppression of viremia to <50 copies/ml on HAART. Patients in the acute cohort started therapy within 3 months of infection.</p>d<p>Time of documented continuous suppression of viremia to <50 copies/ml on HAART.</p>e<p>Drug abbreviations: 3TC, lamivudine; ABC, abacavir; ATV/r, atazanavir boosted with ritonavir; d4T, stavudine; ddI, didanosine; DRV/r, darunavir boosted with ritonavir; EFV, efavirnez; ETV, etravirine; FTC, emtricitabine; FPV, fosamprenavir; FPV/r, fosamprenavir boosted with ritonavir; NVP, nevirapine; RAL, raltegravir; TDF, tenofovir disoproxil fumarate.</p

    Characteristics of assays.

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    a<p>HXB2 coordinates.</p>b<p>Based in standard sample size. Except for residual viremia, LOD is expressed as infectious units or copies per 10<sup>6</sup> cells. For residual viremia, the LOD is 0.2 copies/ml of plasma.</p>c<p>Dynamic range is reported here as the difference in log units between the highest value measured in these study patients and the limit of detection of the relevant assay.</p>d<p>Based on repeat measurements in the same patient as reported in reference 10 and assuming no decay in the reservoir.</p
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