HCMV miR-UL70-3p 通过靶向自噬相关蛋白 9A (ATG9A) 下调雷帕霉素诱导的自噬。

IF 4.3 4区 医学 Q2 IMMUNOLOGY
International Reviews of Immunology Pub Date : 2024-01-01 Epub Date: 2024-01-02 DOI:10.1080/08830185.2023.2296488
Raj Kumar Khalko, Abhishek Pandeya, Sangeeta Saxena, Sunil Babu Gosipatala
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引用次数: 0

摘要

人类巨细胞病毒(HCMV)是一种具有代表性的β-疱疹病毒,可在人体内形成持续感染,在成人中血清阳性率很高。它与人类宿主共同进化,并利用其基因组的重要部分采用各种策略逃避抗病毒机制。HCMV 编码的蛋白质和 miRNA 与调节这些机制有关,从而使病毒能够在人体内存活。在病毒感染期间,自噬是一种保守的分解代谢过程,对细胞的平衡至关重要,是一种抗病毒防御机制。多项研究表明,HCMV 可通过其蛋白质和 miRNAs 调节自噬,从而影响其在宿主体内的存活。在本研究中,我们发现了 HCMV miRNAs 参与细胞自噬的可能性。我们利用各种生物信息学工具预测了靶向自噬相关基因的推定 HCMV miRNA 及其相应的细胞自噬基因。我们的结果表明,自噬相关基因(包括 ATG9A、ATG9B、ATG16L2、SQSTM1 和 EIF2AK2)的 3'UTR 隐藏着 hcmv-miR-UL70-3p 的潜在结合位点。异位表达 hcmv-miR-UL70-3p 的实验操作表明,雷帕霉素诱导的自噬显著减少,ATG9A 是其功能靶点。这些发现证实,hcmv-miR-UL70-3p 通过抑制 ATG9A 的表达,起到了自噬抑制剂的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
HCMV miR-UL70-3p downregulates the rapamycin-induced autophagy by targeting the autophagy-related protein 9A (ATG9A).

Human cytomegalovirus (HCMV) is a representative β-herpesvirus that establishes persistent infections in humans, and exhibits high seropositivity rates in adults. It has co-evolved with its human host and employs various strategies to evade antiviral mechanisms by utilizing a significant portion of its genome. HCMV-encoded proteins and miRNAs have been implicated in regulating these mechanisms, enabling viral survival within the human body. During viral infections, autophagy, a conserved catabolic process essential for cellular homeostasis, acts as an antiviral defense mechanism. Multiple studies have reported that HCMV can modulate autophagy through its proteins and miRNAs, thereby influencing its survival within the host. In this study, we showed the potential involvement of HCMV miRNAs in cellular autophagy. We employed various bioinformatic tools to predict putative HCMV miRNAs that target autophagy-related genes and their corresponding cellular autophagy genes. Our results show that the 3'UTR of autophagy-related genes, including ATG9A, ATG9B, ATG16L2, SQSTM1, and EIF2AK2, harbors potential binding sites for hcmv-miR-UL70-3p. Experimental manipulation involving ectopic expression of hcmv-miR-UL70-3p demonstrated a significant reduction in rapamycin-induced autophagy, with ATG9A as its functional target. These findings establish that hcmv-miR-UL70-3p acts as an autophagy inhibitor by suppressing the expression of ATG9A.

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来源期刊
CiteScore
11.00
自引率
4.00%
发文量
24
期刊介绍: This review journal provides the most current information on basic and translational research in immunology and related fields. In addition to invited reviews, the journal accepts for publication articles and editorials on relevant topics proposed by contributors. Each issue of International Reviews of Immunology contains both solicited and unsolicited review articles, editorials, and ''In-this-Issue'' highlights. The journal also hosts reviews that position the authors'' original work relative to advances in a given field, bridging the gap between annual reviews and the original research articles. This review series is relevant to all immunologists, molecular biologists, microbiologists, translational scientists, industry researchers, and physicians who work in basic and clinical immunology, inflammatory and allergic diseases, vaccines, and additional topics relevant to medical research and drug development that connect immunology to disciplines such as oncology, cardiovascular disease, and metabolic disorders. Covered in International Reviews of Immunology: Basic and developmental immunology (innate and adaptive immunity; inflammation; and tumor and microbial immunology); Clinical research (mechanisms of disease in man pertaining to infectious diseases, autoimmunity, allergy, oncology / immunology); and Translational research (relevant to biomarkers, diagnostics, vaccines, and drug development).
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