Factorial analysis.

<p><b>A)</b> One way ANOVA stratified by alcohol consumption pattern and 3 specific factors: Early Activation (Upper graph), Effector Activation (Middle graph) and Trafficking (Lower graph) <b>B)</b> Association of the factors in a XYZ surface plot, Z axis Trafficking factor, X axis Early Activation factor and Y axis Effector Activation factor. ^a,b,cIndicates homogeneous groups using DMS contrast where a > b > c. ^A,B,CIndicates homogeneous groups using Tamhane contrast where A > B > C.</p

Alcohol consumption patterns modify the peripheral CD8 profile.

<p><b>A)</b> Flow cytometry analysis of a representative sample of peripheral blood leukocytes; CD8 cells were sorted by forward vs. side scatter pattern (left panel) and the expression of CD3 and CD8 (right panel). Quadrants indicate percentage of CD8. Representative expression of the CD8 profile (left panel): CD25⁺CD127⁺<b>(B)</b> and CD127^-CCR5^high<b>(C)</b>. Scatter plot (right panel) summarizing the distribution (mean ± SD) of indicated CD8 phenotype according to alcohol consumption pattern: CD25⁺CD127⁺<b>(B)</b> and CD127^-CCR5^high<b>(C)</b>. ^a,b,cIndicates homogeneous groups using DMS contrast where a > b > c.</p

Alcohol consumption patterns modify the expression of CD69 and TLR4 in peripheral CD8.

<p>Representative FACS histograms for MFI of CD69 (upper panel) and TLR4 (lower panel) in peripheral CD8 population. MFI comparison of control (as FMO) and alcohol consumption groups (left panel). Scatter plot (right panel) summarizing the MFI of CD69 (upper panel) and TLR4 (lower panel) separated by alcohol consumption pattern. FMO: fluorescence minus one. ^a,b,cIndicates homogeneous groups using Tamhane contrast where a > b > c.</p

Clinical and demographic characteristics of participants according to their drinking pattern.

<p>^a,b,c Indicate homogeneous groups contrast, where a > b > c.</p><p>^¥ Chi-squared Test.</p><p>^& One-way ANOVA DMS post-hoc test.</p><p>^€ One-way ANOVA Tamhane post-hoc test.</p><p>Clinical and demographic characteristics of participants according to their drinking pattern.</p

Measure loadings after varimax rotation of first three components of principal component analysis.

<p>Rotated factor loadings variables of activation, trafficking and cytotoxicity settings were used to conform the components as described in Material and Methods.</p

Immunophenotyping of peripheral T-CD8 participants according to their drinking pattern.

<p>^a,b,c Indicate homogeneous groups contrast, where a > b > c.</p><p>^&One-way ANOVA DMS post-hoc test.</p><p>^€One-way ANOVA Tamhane post-hoc test.</p><p>Immunophenotyping of peripheral T-CD8 participants according to their drinking pattern.</p

High HPgV replication is associated with improved surrogate markers of HIV progression

<div><p>Background</p><p>Human Pegivirus (HPgV) may have a beneficial effect on HIV disease progression in co-infected patients; however, the virologic characteristics of this infection are not well defined. In this study, we determined HPgV viremia prevalence in Mexico and provide new insights to understand HPgV infection and HPgV/HIV co-infection.</p><p>Methods</p><p>We analyzed and quantified 7,890 serum samples for HPgV viremia by One-Step RT-Real-Time PCR, 6,484 from healthy blood donors and 1,406 from HIV-infected patients. Data on HIV progression were obtained from patients’ records. HPgV genotyping was performed in 445 samples by nested PCR of the 5’URT region. Finite Mixture Models were used to identify clustering patterns of HPgV viremia in blood donors and co-infected antiretroviral (ART)-naïve patients.</p><p>Results</p><p>HPgV was detected in 2.98% of blood donors and 33% of HIV patients, with a wide range of viral loads. The most prevalent genotypes were 3 (58.6%)and 2 (33.7%). HPgV viral loads from healthy blood donors and HPgV/HIV+ ART-naïve co-infected patients were clustered into two component distributions, low and high, with a cut-off point of 5.07log₁₀ and 5.06log₁₀, respectively. High HPgV viremia was associated with improved surrogate markers of HIV infection, independent of the estimated duration of HIV infection or HIV treatment.</p><p>Conclusions</p><p>HPgV prevalence in Mexico was similar to that reported for other countries. The prevalent genotypes could be related to Mexico’s geographic location and ethnicity, since genotype 2 is frequent in the United States and Europe and genotype 3 in Asia and Amerindian populations. HPgV viral load demonstrated two patterns of replication, low and high. The more pronounced beneficial response observed in co-infected patients with high HPgV viremia may explain discrepancies found between other studies. Mechanisms explaining high and low HPgV replication should be explored to determine whether the persistently elevated replication depends on host or viral factors.</p></div

Mean difference of HIV viral load in co-infected subjects according to time of HIV infection and HPgV viral load conditions.

<p>Mean difference of HIV viral load in co-infected subjects according to time of HIV infection and HPgV viral load conditions.</p

Effects of HPgV genotype (2 or 3) on surrogate markers of HIV progression.

<p>Each graph shows the differences between the means of: (A and B) HIV viral load/ml (log₁₀), (C and D) CD4⁺ cell counts (CD4⁺/mm³), and (E and F) CD4⁺/CD8⁺ ratio, in the ART-naïve population according to their HPgV condition (-negative, -low, or -high) and genotype 3 (A, C and E) and genotype 2 (B, D and F). Significant differences are considered at p<0.05.</p

Mean difference of CD4⁺/CD8⁺ ratio in co-infected subjects according to time of HIV infection and HPgV viral load condition.

<p>Mean difference of CD4⁺/CD8⁺ ratio in co-infected subjects according to time of HIV infection and HPgV viral load condition.</p