Abstract
BackgroundHuman 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.MethodsWe 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.ResultsHPgV 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.ConclusionsHPgV 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.
Highlights
Human Pegivirus (HPgV), formerly GB virus C (GBV-C), was considered non-pathogenic, this concept has changed due to its association with non-Hodgkin’s lymphoma [1,2]
High HPgV viremia is associated with reduced HIV progression into two component distributions, low and high, with a cut-off point of 5.07log10 and 5.06log10, respectively
The more pronounced beneficial response observed in co-infected patients with high HPgV viremia may explain discrepancies found between other studies
Summary
Human Pegivirus (HPgV), formerly GB virus C (GBV-C), was considered non-pathogenic, this concept has changed due to its association with non-Hodgkin’s lymphoma [1,2]. HPgV is classified in the genus Pegivirus within the Flaviviridae and it is the most prevalent flavivirus in the world [3]. The prevalence of HPgV viremia is 1–5% among healthy blood donors, higher prevalences have been found in developing countries (up to 18%) [4] Co-infection with HPgV occurs in 20–40% of HIV patients; both viruses share transmission routes: blood transfusion, sexual and vertical [5,6,7,8]. Several studies have shown that co-infected patients have slower HIV progression, increased survival time, and decreased vertical HIV transmission, all of these described as HPgV beneficial effects. Human Pegivirus (HPgV) may have a beneficial effect on HIV disease progression in coinfected patients; the virologic characteristics of this infection are not well defined. We determined HPgV viremia prevalence in Mexico and provide new insights to understand HPgV infection and HPgV/HIV co-infection
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