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在分娩时,病毒抑制的感染 HIV-1 的喀麦隆孕妇的血浆和胎盘中的 miR3181 和 miR199a 的表达谱。

Expression profiles of miR3181 and miR199a in plasma and placenta of virally suppressed HIV-1 infected Cameroonian pregnant women at delivery.

机构信息

The Biotechnology Center, University of Yaounde I, Yaounde, Cameroon.

Centre for Medical Research, Institute Medical Research and Medicinal Plant Studies, Yaounde, Cameroon.

出版信息

PLoS One. 2022 May 20;17(5):e0268820. doi: 10.1371/journal.pone.0268820. eCollection 2022.

DOI:10.1371/journal.pone.0268820
PMID:35594307
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9122233/
Abstract

Human immunodeficiency virus (HIV)-1 infection during pregnancy reduces the transplacental transfer of protective maternal antibodies needed to confer immunity during early postnatal life. However, the mediation of MicroRNA in this dysregulation is not well understood MicroRNAs 3181 and 199a have been shown to mediate neonatal Fc receptor (FcRn)-like transmembrane antibody transfer and endocytosis respectively but their expression levels in the placenta and plasma in women living with HIV have not been extensively investigated. The objective of this study was to determine how the expression levels of miR-3181 and miR-199a in the placenta and plasma are affected in women chronically infected with HIV who are on antiretroviral therapy (ART) and are virally suppressed at delivery. In this pilot case-control study, plasma and placenta biopsies were obtained from 36 (18 HIV+ and 18 HIV-) Cameroonian women at delivery. MicroRNAs 3181 and 199a expression levels were measured using RT-qPCR, data was analyzed using SPSS22.0 and R 3.60, and p values below 0.05 were considered statistically significant. All the HIV-infected women were on known ART regimens and were virally suppressed. There was no significant difference in the levels of miR-3181 (p>0.05) in the placenta and plasma amongst HIV-infected and HIV uninfected women. The expression levels of miR-199a were significantly greater in the plasma compared to the placenta of HIV+ (p = 0.00005) and HIV- (p = 0.027) women. Moreover, there was a significantly higher (p = 0.02) level of miR-199a in the plasma of women with HIV and their uninfected counterparts. Linear regression models adjusted for systolic pressure showed no significant difference (p>0.05) in the levels of miR-199a and miR-3181 in both the placenta and plasma due to HIV infection. Our findings suggest that even though ART uptake and viral suppression might help in maintaining miR3181 and miR199a levels in the placenta of women with HIV at comparative levels to those of their HIV negative counterparts, the significantly higher levels of miR-199a in the plasma of women with HIV compared to the placenta might highlight lurking systemic dangers and requires further investigation.

摘要

人类免疫缺陷病毒(HIV)-1 感染会降低母体抗体通过胎盘的转移,而这些抗体是新生儿在生命早期获得免疫所必需的。然而,MicroRNA 在这种失调中的介导作用还不太清楚。MicroRNA 3181 和 199a 已被证明分别介导新生儿 Fc 受体(FcRn)样跨膜抗体转移和内吞作用,但它们在 HIV 感染者胎盘和血浆中的表达水平尚未得到广泛研究。本研究的目的是确定在接受抗逆转录病毒治疗(ART)且在分娩时病毒得到抑制的慢性 HIV 感染妇女中,胎盘和血浆中 miR-3181 和 miR-199a 的表达水平如何受到影响。在这项初步的病例对照研究中,从喀麦隆 36 名妇女(18 名 HIV+和 18 名 HIV-)分娩时获得了血浆和胎盘活检。使用 RT-qPCR 测量 MicroRNAs 3181 和 199a 的表达水平,使用 SPSS22.0 和 R 3.60 分析数据,p 值低于 0.05 被认为具有统计学意义。所有感染 HIV 的妇女均接受已知的 ART 方案治疗,病毒得到抑制。在感染 HIV 和未感染 HIV 的妇女中,胎盘和血浆中 miR-3181 的水平没有显著差异(p>0.05)。与 HIV+(p=0.00005)和 HIV-(p=0.027)妇女的胎盘相比,血浆中 miR-199a 的表达水平显著更高。此外,HIV 阳性妇女及其未感染对照妇女的血浆中 miR-199a 水平显著更高(p=0.02)。调整收缩压的线性回归模型显示,由于 HIV 感染,胎盘和血浆中 miR-199a 和 miR-3181 的水平没有显著差异(p>0.05)。我们的研究结果表明,尽管接受抗逆转录病毒治疗和病毒抑制可能有助于维持 HIV 感染者胎盘内 miR3181 和 miR199a 的水平与未感染 HIV 的妇女相当,但与胎盘相比,HIV 感染者血浆中 miR-199a 的水平显著升高可能凸显出潜在的全身危险,需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e1d/9122233/5df689f197ad/pone.0268820.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e1d/9122233/b6a3140d320f/pone.0268820.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e1d/9122233/cce6de4354f4/pone.0268820.g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e1d/9122233/5df689f197ad/pone.0268820.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e1d/9122233/b6a3140d320f/pone.0268820.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e1d/9122233/cce6de4354f4/pone.0268820.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e1d/9122233/5fb42e72edab/pone.0268820.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e1d/9122233/5df689f197ad/pone.0268820.g004.jpg

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