Cellular miR-101-1 Reduces Efficiently the Replication of HSV-1 in HeLa Cells.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2021-01-01 Epub Date: 2021-02-24 DOI:10.1159/000512956
Bahar Sadegh Ehdaei, Ahmad Pirouzmand, Mehdi Shabani, Arezoo Mirzaei, Sharareh Moghim
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引用次数: 5

Abstract

Introduction: Herpes simplex viruses (HSVs) are widely distributed in the human population. HSV type 1 (HSV-1) is responsible for a spectrum of diseases, ranging from gingivostomatitis to keratoconjunctivitis, and encephalitis. The HSVs establish latent infections in nerve cells, and recurrences are common. Their frequent reactivation in elderly and immunosuppressed patients causes serious health complications.

Objectives: Due to the growing resistance to its main drug, acyclovir, alternative treatments with different mechanisms of action are required. MicroRNAs regulate host and viral gene expression posttranscriptionally. Previous studies reported that mir-101-2 expression has widely participated in the regulation of HSV-1 replication. In this study, we investigate the effect of hsa-miR-101-1 in the replication of HSV-1.

Methods: We found that transfection of miR-101-1 into HeLa cells could reduce effectively HSV-1 replication using plaque assay and real-time PCR methods.

Results: We showed that overexpression of miR-10-1 produced less viral progeny and manifested a weaker cytopathic effect, without affecting cell viability.

Discussion/conclusion: This result can give us new insights into the control of HSV-1 infections.

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细胞miR-101-1有效降低HSV-1在HeLa细胞中的复制
简介:单纯疱疹病毒(hsv)广泛分布于人群中。HSV 1型(HSV-1)是一系列疾病的罪魁祸首,从牙龈口炎到角膜结膜炎和脑炎。单纯疱疹病毒在神经细胞中建立潜伏感染,复发是常见的。它们在老年人和免疫抑制患者中频繁的再激活会导致严重的健康并发症。目的:由于对其主要药物阿昔洛韦的耐药性日益增加,需要不同作用机制的替代治疗。MicroRNAs通过转录后调控宿主和病毒基因的表达。既往研究报道,mir-101-2的表达广泛参与了HSV-1复制的调控。在这项研究中,我们研究了hsa-miR-101-1在HSV-1复制中的作用。方法:通过斑块测定和实时PCR方法,我们发现转染miR-101-1到HeLa细胞可以有效地减少HSV-1的复制。结果:我们发现过表达miR-10-1产生的病毒子代较少,细胞病变作用较弱,不影响细胞活力。讨论/结论:这一结果为我们控制1型单纯疱疹病毒感染提供了新的见解。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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