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细胞 miR-101-1 可有效降低 HSV-1 在 HeLa 细胞中的复制。

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

机构信息

Department of Microbiology, Kashan University of Medical Sciences, Kashan, Iran.

Autoimmune Diseases Research Center, Faculty of Medicine, Kashan University of Medical Sciences, Kashan, Iran.

出版信息

Intervirology. 2021;64(2):88-95. doi: 10.1159/000512956. Epub 2021 Feb 24.

DOI:10.1159/000512956
PMID:33626544
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.

摘要

简介

单纯疱疹病毒(HSV)广泛存在于人群中。单纯疱疹病毒 1 型(HSV-1)可引起多种疾病,从龈口炎到角膜炎和脑炎。HSV 在神经细胞中建立潜伏感染,复发较为常见。其在老年和免疫抑制患者中的频繁再激活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不断增加,需要具有不同作用机制的替代治疗方法。微小 RNA 在后转录水平上调节宿主和病毒基因的表达。先前的研究报道,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

我们发现 miR-101-1 的转染可以通过噬斑试验和实时 PCR 方法有效降低 HSV-1 的复制。

结果

我们表明,miR-10-1 的过表达产生的病毒子代较少,表现出较弱的细胞病变效应,而不影响细胞活力。

讨论/结论:这一结果可以为我们控制 HSV-1 感染提供新的思路。

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