17 research outputs found
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 patientsâ records. HPgV genotyping was performed in 445 samples by nested PCR of the 5âURT region. Finite Mixture Models were used to identify clustering patterns of HPgV viremia in blood donors and co-infected antiretroviral (ART)-naĂŻve 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-naĂŻve co-infected patients were clustered into two component distributions, low and high, with a cut-off point of 5.07log<sub>10</sub> and 5.06log<sub>10</sub>, 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 Mexicoâs 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 (log<sub>10</sub>), (C and D) CD4<sup>+</sup> cell counts (CD4<sup>+</sup>/mm<sup>3</sup>), and (E and F) CD4<sup>+</sup>/CD8<sup>+</sup> ratio, in the ART-naĂŻve 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<sup>+</sup>/CD8<sup>+</sup> ratio in co-infected subjects according to time of HIV infection and HPgV viral load condition.
<p>Mean difference of CD4<sup>+</sup>/CD8<sup>+</sup> ratio in co-infected subjects according to time of HIV infection and HPgV viral load condition.</p
Diagram of pooling method for serum samples from blood donors.
<p>The diagram shows the construction of sample pools and analysis for HPgV viremia in healthy blood donors. Positive samples from the pool were re-tested in smaller pools each time until we detected the positive individual donor sample.</p
Mean difference of CD4<sup>+</sup> cell counts (CD4<sup>+</sup>/mm<sup>3</sup>) in co-infected subjects according to time of HIV infection and HPgV viral load conditions.
<p>Mean difference of CD4<sup>+</sup> cell counts (CD4<sup>+</sup>/mm<sup>3</sup>) in co-infected subjects according to time of HIV infection and HPgV viral load conditions.</p
Two-component cluster mixture model fit for weighted HPgV viral load from healthy blood donors and co-infected ART-naĂŻve patients.
<p>Density distribution (bars) of HPgV viral load (log<sub>10</sub> genome equivalents) from healthy blood donors (A) and co-infected ART-naĂŻve patients (B). Gaussian curves indicate the fitted low (red line), high (green line), mean component curves (ÎŒ), the number of patients (n) and proportion (λ) in each population component. The clustersâ cut-off point for healthy blood donors (A) and co-infected ART-naĂŻve patients (B), is the intersection of the curves.</p
Surrogate markers of HIV progression compared between genotypes 2 and 3, according to the low or high HPgV viral loads in HIV-positive ART-naĂŻve patients.
<p>Surrogate markers of HIV progression compared between genotypes 2 and 3, according to the low or high HPgV viral loads in HIV-positive ART-naĂŻve patients.</p
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
Known-groups validity: FLU-PRO scores by patient global rating of disease severity, Day 1.
<p>Known-groups validity: FLU-PRO scores by patient global rating of disease severity, Day 1.</p