Kaplan-Meier survival curves related to the free-of-therapy period.

<p>The survival analysis was performed considering the time elapsed from PHI to the occurrence of failure, defined as the start of antiretroviral therapy. Upper pane, all patients; lower panels, patients with different degree of CD8+ T cell activation.</p

Trends of the Treg frequency (upper panel), absolute number (middle panel) and activated Treg (lower panel), in the patients under investigation.

<p>Tregs were considered as those cells that were CD3+,CD4+, positive to FoxP3, highly positive (<i>i.e.</i>, bright) to CD25 and negative to CD127. Boxes indicate median values with 25th and 75th percentiles, whiskers show minimum and maximum.</p

Characterization of the T cell response to gag-derived peptides.

<p>Pie charts show the qualitative composition of total gag-specific CD4+ or CD8+ T cell response; each pie slice represents the mean proportion of the total CD4+ T cell response contributed by a single functional pattern, as indicated in the bottom legend. Arcs designed outside the pies represent the fraction of total cells expressing a particular marker, irrespectively of the positive or negative expression of other markers (blue: CD154; red: CD107a; green: IFN-γ; black: IL-2).</p

Correlation between the level of CD4+ T cell activation status and pVL levels, at all months analyzed.

<p>Activated cells were identified as described in the legend to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0050728#pone-0050728-g006" target="_blank">Figure 6</a>.</p

Trends of CD8+ T and CD4+ T cell response to gag- and nef-derived peptides.

<p>Boxes indicate median values with 25th and 75th percentiles, whiskers show minimum and maximum. Figure shows the total response to viral peptides, <i>i.e.</i>, the sum of all cells positive for at least one of the markers studied (IL-2, IFN-γ, CD154 and CD107a). Patients were studied at month 1 (M1), month 2 (M2), month 3 (M3), month 4 (M4), and month 6 (M6) after PHI. The values of nonparametric analysis of variance (Skillings-Mack, and p values) are reported in figures. Stars in graphs indicate the significant differences of pairwise comparisons between the indicated months, performed by Tukey-Kramer test.</p

Kinetics of changes in CD4+ T cell count (cell/µL blood, upper panel) and plasma viral load (pVL, number of copies/mL blood, lower panel) after primary HIV infection.

<p>Each patients is represented by a different colour.</p

Percentages of activated CD4+ (upper panel) and CD8+ (lower panel) T cells.

<p>Activated cells were considered those expressing high levels of CD38 (CD38 bright) and MHC class II (HLA-DR) molecules. Boxes indicate median values with 25th and 75th percentiles, whiskers show minimum and maximum.</p

Association between CD4+ or CD8+ T cell activation at M2 and M3 and the length of the period free of therapy.

<p>Activated cells were identified as described in the legend to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0050728#pone-0050728-g006" target="_blank">Figure 6</a>.</p

Characterization of the T cell response to nef-derived peptides.

<p>Pie charts show the qualitative composition of total gag-specific CD4+ or CD8+ T cell response; each pie slice represents the mean proportion of the total CD4+ T cell response contributed by a single functional pattern, as indicated in the bottom legend. Arcs designed outside the pies represent the fraction of total cells expressing a particular marker, irrespectively of the positive or negative expression of other markers (blue: CD154; red: CD107a; green: IFN-γ; black: IL-2).</p

COVID-19 Host Genetics Initiative. A first update on mapping the human genetic architecture of COVID-19

The COVID-19 pandemic continues to pose a major public health threat, especially in countries with low vaccination rates. To better understand the biological underpinnings of SARS-CoV-2 infection and COVID-19 severity, we formed the COVID-19 Host Genetics Initiative1. Here we present a genome-wide association study meta-analysis of up to 125,584 cases and over 2.5 million control individuals across 60 studies from 25 countries, adding 11 genome-wide significant loci compared with those previously identified2. Genes at new loci, including SFTPD, MUC5B and ACE2, reveal compelling insights regarding disease susceptibility and severity.</p