Horemheb-Rubio Gibran, Ramos-Cervantes Pilar, Arroyo-Figueroa Hugo, Ávila-Ríos Santiago, García-Morales Claudia, Reyes-Terán Gustavo, Escobedo Galileo, Estrada Gloria, García-Iglesias Trinidad, Muñoz-Saucedo Nayeli, Kershenobich David, Ostrosky-Wegman Patricia, Ruiz-Palacios Guillermo M
Department of Infectious Diseases, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Infectious Diseases Research Center, Instituto Nacional de Enfermedades Respiratorias, Mexico City, Mexico.
PLoS One. 2017 Sep 14;12(9):e0184494. doi: 10.1371/journal.pone.0184494. eCollection 2017.
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.
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.
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.
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.
人佩吉病毒（HPgV）可能对合并感染患者的HIV疾病进展具有有益作用；然而，这种感染的病毒学特征尚未明确界定。在本研究中，我们确定了墨西哥的HPgV病毒血症患病率，并为理解HPgV感染及HPgV/HIV合并感染提供了新的见解。
我们采用一步法逆转录实时荧光定量PCR对7890份血清样本进行分析和定量检测HPgV病毒血症，其中6484份来自健康献血者，1406份来自HIV感染患者。从患者记录中获取HIV疾病进展的数据。通过对5'URT区域进行巢式PCR，对445份样本进行HPgV基因分型。使用有限混合模型来识别献血者和未接受抗逆转录病毒治疗（ART）的合并感染患者中HPgV病毒血症的聚集模式。
在2.98%的献血者和33%的HIV患者中检测到HPgV，病毒载量范围广泛。最常见的基因型是3型（58.6%）和2型（33.7%）。健康献血者和未接受ART治疗的HPgV/HIV合并感染患者的HPgV病毒载量聚为两个成分分布，即低水平和高水平，截断点分别为5.07log10和5.06log10。高HPgV病毒血症与HIV感染的替代指标改善相关，与估计的HIV感染持续时间或HIV治疗无关。
墨西哥的HPgV患病率与其他国家报告的相似。流行的基因型可能与墨西哥的地理位置和种族有关，因为2型在美国和欧洲较为常见，而3型在亚洲和美洲印第安人群体中较为常见。HPgV病毒载量表现出低水平和高水平两种复制模式。在高HPgV病毒血症的合并感染患者中观察到的更明显的有益反应可能解释了其他研究中发现的差异。应探索解释HPgV高复制和低复制的机制，以确定持续升高的复制是否取决于宿主或病毒因素。
