Demographics, clinical details and CD4+ count variability of patients with suppressed HIV infection on ART and untreated HIV infection.^§

<p>^†Patients with active HCV or HBV infection were excluded. Patients were on ART for a minimum of 3 years and had reached a plateau in their CD4+ T cell counts.</p><p>^§Legend: Coefficient of variation (CV); standard deviation (SD); interquartile range (IQR);</p><p>* p <0.01 when compared to treated HIV infection; Duration of cART was calculated from the date cART started to the date of the first CD4+ measurement used in the analysis.</p><p>Demographics, clinical details and CD4+ count variability of patients with suppressed HIV infection on ART and untreated HIV infection.<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0125248#t001fn002" target="_blank">^§</a></p

Estimated range of absolute and percent CD4+ T cell counts with a single determination The predicted confidence limits of absolute and percent CD4+ T cell count based on a single recorded CD4+ T cell measurement from 88 HIV-infected individuals (same cohort as in Fig 1).

<p>Sixty-eight % of mean absolute or percent CD4+ T cell counts will fall within ± 1 standard deviation (SD) from the mean; 95% of mean absolute or percent CD4+ T cell counts will fall within ± 2 SD from the mean.</p

Comparison of innate and adaptive IFN-γ production ex vivo with horizontal error bars representing the median and interquartile range.

<p>A. HIV-uninfected controls and HIV infected participants B. HIV-uninfected controls and HIV-infected participants on and off ART.</p

Innate and adaptive IFN-γ production ex vivo in HIV infected participants with horizontal error bars representing the median and interquartile range.

<p>A. CD4 count in treated participants, B. sex, C. duration of HIV infection and D. nadir CD4 count.</p

Kaplan-Meier plots showing time taken to achieve CD4 T-cell counts &gt;500 cells/µl following cART initiation.

<p>Kaplan-Meier plots showing time taken to achieve CD4 counts &gt;500cells/µl among (A) patients in the total cohort (n = 501) and patients with no evidence of virological failure (VF) (2 consecutive HIV RNA&gt;500copies/ml) throughout follow-up (n = 331) and (B) all patients (n = 501) stratified by baseline CD4 T-cell counts (&lt;100cells/µl, n = 99; 101–200cells/µl, n = 107; 201–350cells/µl, n = 172; &gt;350cells/µl, n = 123). Comparisons of survival curves were done using the Log-rank test (STATA 10.0).</p

Patient disposition.

<p>Patient disposition.</p

Predictors of time taken to achieve CD4 T-cells &gt;200 cells/µl (n = 196).

<p>*Reference category.</p><p>**Others included injecting drug use, transfusion and unrecorded.</p><p>cART-combination Antiretroviral therapy; MSM – men who have sex with men; NNRTI – non-nucleoside reverse transcriptase inhibitor; PI – protease inhibitor (boosted and unboosted) ; NRTI – nucleoside reverse transcriptase inhibitor; ADI – AIDS-defining illness; HBsAg – hepatitis B surface antigen; HCV Ab – hepatitis C antibody.</p

Demographic and clinical characteristics of patients from AHOD who met the inclusion criteria for this study.

<p>All parameters are median (IQR) unless otherwise stated.</p><p>cART-combination Antiretroviral therapy; MSM – men who have sex with men; NNRTI – non-nucleoside reverse transcriptase inhibitor; PI – protease inhibitor (boosted and unboosted); NRTI – nucleoside reverse transcriptase inhibitor.</p><p>*Others included injecting drug use, transfusion and unrecorded.</p><p>PIs included Atazanavir (boosted and unboosted) (5%), Lopinavir/Ritonavir (11%), Indinavir (boosted and unboosted) (32%), Nelfinavir (27%), Ritonavir (10%), Saquinavir (boosted and unboosted) (13%), Tipranavir (1%), Fosamprenavir (1%); NNRTIs included Delavirdine (1%), Efavirenz (44%), Nevirapine(55%);</p

Predictors of time taken to achieve CD4 T-cells &gt;500 cells/µl (n = 501).

<p>*Reference category.</p><p>**Others included injecting drug use, transfusion and unrecorded.</p>#<p>For every 100-unit increase in square transformed baseline CD4 T-cell counts, the hazard of achieving a CD4 T-cell threshold of &gt;500cells/µl increased by 15%.</p><p>cART-combination Antiretroviral therapy; MSM – men who have sex with men; NNRTI – non-nucleoside reverse transcriptase inhibitor; PI – protease inhibitor (boosted and unboosted) ; NRTI – nucleoside reverse transcriptase inhibitor; ADI – AIDS-defining illness; HBsAg – hepatitis B surface antigen; HCV Ab – hepatitis C antibody.</p

Latency is established with higher efficiency following co-culture of resting CD4+ T-cells with mDC.

<p>Resting CD4+ T-cells from 2 donors were labelled with eFluor670 cytoplasmic dye and cultured for 24 hours either untreated (<i>red</i>), with 100 nM CCL19 (<i>purple</i>) or with autologous mDCs at 1 mDC:10 T-cell ratio (<i>blue</i>). Cells were incubated with increasing TCID₅₀ per cell of X4-tropic HIV^NL4.3-EGFP. After 2 hours, cells were washed, cultured for 5 days in a low concentration of IL-2 (2 U/ml) and analysed for EGFP expression by flow cytometry to quantify productive infection (A). Additionally, non-proliferating eFluor670^hiEGFP- cells were sorted, cultured for 3 days with anti-CD3/anti-CD28 plus IL-7, in the presence of the integrase inhibitor L-870812 (L8), to induce EGFP expression from post-integration latent infection (B). As a comparative control, aliquots of sorted cells were also cultured for 3 days with L-870812 (L8) but no reactivation stimuli in order to measure background, spontaneous EGFP expression during 3 further days of culture (C). The true level of post-integrated latency in cultures was calculated by subtracting the percentage of EGFP+ cells in the spontaneous cultures from the percentage of EGFP+ cells in reactivated cultures (D). The percentage of EGFP+ cells per 10⁴ cultured cells is shown. Columns represent the median of donor pairs with each donor shown as a different symbol.</p