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Cloning and identification of a microRNA cluster within the latency-associated region of Kaposi's sarcoma-associated herpesvirus 总被引:13,自引:0,他引:13 下载免费PDF全文
MicroRNAs (miRNAs) are small, noncoding regulatory RNA molecules that bind to 3' untranslated regions (UTRs) of mRNAs to either prevent their translation or induce their degradation. Previously identified in a variety of organisms ranging from plants to mammals, miRNAs are also now known to be produced by viruses. The human gammaherpesvirus Epstein-Barr virus has been shown to encode miRNAs, which potentially regulate both viral and cellular genes. To determine whether Kaposi's sarcoma-associated herpesvirus (KSHV) encodes miRNAs, we cloned small RNAs from KSHV-positive primary effusion lymphoma-derived cells and endothelial cells. Sequence analysis revealed 11 isolated RNAs of 19 to 23 bases in length that perfectly align with KSHV. Surprisingly, all candidate miRNAs mapped to a single genomic locale within the latency-associated region of KSHV. These data suggest that viral and host cellular gene expression may be regulated by miRNAs during both latent and lytic KSHV replication. 相似文献
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MicroRNAs (miRNAs) mark a new paradigm of RNA-directed gene expression regulation in a wide spectrum of biological systems. These small non-coding RNAs can contribute to the repertoire of host-pathogen interactions during viral infection. This interplay has important consequences, both for the virus and the host. There have been reported evidences of host-cellular miRNAs modulating the expression of various viral genes, thereby playing a pivotal role in the host–pathogen interaction network. In the hide-and-seek game between the pathogens and the infected host, viruses have evolved highly sophisticated gene-silencing mechanisms to evade host-immune response. Recent reports indicate that virus too encode miRNAs that protect them against cellular antiviral response. Furthermore, they may exploit the cellular miRNA pathway to their own advantage. Nevertheless, our increasing knowledge of the host–virus interaction at the molecular level should lead us toward possible explanations to viral tropism, latency and oncogenesis along with the development of an effective, durable and nontoxic antiviral therapy. Here, we summarize the recent updates on miRNA-induced gene-silencing mechanism, modulating host–virus interactions with a glimpse of the miRNA-based antiviral therapy for near future. 相似文献
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MicroRNAs (miRNAs) are a large class of approximately 22-nucleotide non-coding RNAs that facilitate mRNA cleavage and translation repression through the RNA interference pathway. Until recently, miRNAs have been exclusively found in eukaryotic organisms. A non-immunogenic molecule requiring minimal genomic investment, these RNAs may offer an efficient means for viruses to modulate both their own and the host's gene expression during a productive viral infection. In this study we report that human cytomegalovirus (HCMV) expresses miRNAs during its productive lytic infection of four clinically relevant human cell types: fibroblast, endothelial, epithelial and astrocyte cells. The sequences of the miRNAs, expressed from the UL23 and US24 loci of the viral genome, were conserved among all HCMV strains examined and in chimpanzee cytomegalovirus. Furthermore, their expression was detected from both a laboratory-adapted strain and a clinical isolate of HCMV. The conservation of these miRNAs and their expression in different cell types suggests that they represent an evolutionarily primitive feature in the viral genome, and that virus-encoded miRNAs may be more common than previously believed. 相似文献
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《Cell cycle (Georgetown, Tex.)》2013,12(22):3595-3600
MicroRNAs (miRNAs) are a large class of small (~22 nt) non-coding RNAs that negatively regulate gene expression most often at the level of translation, and have been shown to be key regulators in a variety of processes including development, cell cycle and immunity. The Epstein-Barr virus (EBV) is an oncogenic herpes virus endemic in humans that encodes at least twenty-two of its own miRNAs. Cellular miRNAs have well-established roles in cancer and immune pathways, and multiple cellular miRNAs directly target viral messages. Additionally, multiple viruses express suppressors of cellular RNAi-induced silencing. Here we show that EBV de novo infection of primary cultured human B-cells results in a dramatic down-regulation of cellular miRNA expression, suggesting the virus may encode or activate a suppressor of miRNA expression. We additionally show that the immuno-modulatory microRNA miR-146a, down-regulated on initial infection, is significantly up-regulated more than 100-fold upon induction of the viral lytic cycle, and appears to have inhibitory effects on the progression of the lytic cycle. Our results show that EBV has large effects on cellular miRNA expression. 相似文献
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Adenovirus infection has a tremendous impact on the cellular silencing machinery. Adenoviruses express high amounts of non-coding virus associated (VA) RNAs able to saturate key factors of the RNA interference (RNAi) processing pathway, such as Exportin 5 and Dicer. Furthermore, a proportion of VA RNAs is cleaved by Dicer into viral microRNAs (mivaRNAs) that can saturate Argonaute, an essential protein for miRNA function. Thus, processing and function of cellular miRNAs is blocked in adenoviral-infected cells. However, viral miRNAs actively target the expression of cellular genes involved in relevant functions such as cell proliferation, DNA repair or RNA regulation. Interestingly, the cellular silencing machinery is active at early times post-infection and can be used to control the adenovirus cell cycle. This is relevant for therapeutic purposes against adenoviral infections or when recombinant adenoviruses are used as vectors for gene therapy. Manipulation of the viral genome allows the use of adenoviral vectors to express therapeutic miRNAs or to be silenced by the RNAi machinery leading to safer vectors with a specific tropism. This article is part of a "Special Issue entitled:MicroRNAs in viral gene regulation". 相似文献
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Virus-encoded microRNAs: novel regulators of gene expression 总被引:15,自引:0,他引:15
MicroRNAs (miRNAs) are a class of small RNAs that have recently been recognized as major regulators of gene expression. They influence diverse cellular processes ranging from cellular differentiation, proliferation, apoptosis and metabolism to cancer. Bioinformatic approaches and direct cloning methods have identified >3500 miRNAs, including orthologues from various species. Experiments to identify the targets and potential functions of miRNAs in various species are continuing but the recent discovery of virus-encoded miRNAs indicates that viruses also use this fundamental mode of gene regulation. Virus-encoded miRNAs seem to evolve rapidly and regulate both the viral life cycle and the interaction between viruses and their hosts. 相似文献
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MicroRNAs (miRNAs) are small non-coding RNAs that control a multitude of critical processes in mammalian cells. Increasing evidence has emerged that host miRNAs serve in animal cells to restrict viral infections. In turn, many viruses encode RNA silencing suppressors (RSS) which are employed to moderate the potency of the cell's miRNA selection against viral replication. Some viruses also encode viral miRNAs. In this review, we summarize findings from human immunodeficiency virus type 1 (HIV-1) and human T-cell leukemia virus type 1 (HTLV-1) that illustrate examples of host cell miRNAs that target the viruses, of RSS encoded by viruses, and of host cell miRNA profile changes that are seen in infected cells. This article is part of a Special Issue entitled: MicroRNAs in viral gene regulation. 相似文献
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疱疹病毒编码的miRNAs的研究进展 总被引:2,自引:0,他引:2
MicroRNAs (miRNAs)是一类长约22个核苷酸的RNA,在数量、序列、结构、表达和功能上具有多样性。目前,通过生物信息学手段和分子克隆方法,已发现了3518种miRNAs,在控制细胞的生长发育、分化、凋亡等过程中发挥着十分重要的作用。最近研究发现某些病毒基因组也能够编码miRNAs,其中大部分为疱疹病毒,这些miRNAs在调控病毒自身表达以及病毒与宿主相互作用方面可能起到重要的作用。找出病毒可能编码的miRNAs,探索其对病毒感染、复制、表达的作用,有助于病毒分子生物学的研究,也会为研发防治病毒的新方法和新途径提供新的思路。 相似文献
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Cellular microRNA let-7c inhibits M1 protein expression of the H1N1 influenza A virus in infected human lung epithelial cells 总被引:1,自引:0,他引:1
Ma YJ Yang J Fan XL Zhao HB Hu W Li ZP Yu GC Ding XR Wang JZ Bo XC Zheng XF Zhou Z Wang SQ 《Journal of cellular and molecular medicine》2012,16(10):2539-2546
The influenza virus (IV) triggers a series of signalling events inside host cells and induces complex cellular responses. Studies have suggested that host factors play an essential role in IV replication. MicroRNAs (miRNAs) represent a class of small non-coding RNAs that target mRNAs, triggering either translation repression or RNA degradation. Emerging research suggests that host-derived cellular miRNAs are involved in mediating the host-IV interaction. Using miRNA microarrays, we identified several miRNAs aberrantly expressed in IV-infected human lung epithelial cells (A549). Specifically, miR-let-7c was highly up-regulated in IV-infected A549 cells. PITA and miRanda database screening indicated that the let-7c seed sequence is a perfect complementary sequence match to the 3' untranslated region (UTR) of viral gene M1 (+) cRNA, but not to PB2 and PA. As detected by a luciferase reporter system, let-7c directly targeted the 3'-UTR of M1 (+) cRNA, but not PB2 and PA. To experimentally identify the function of cellular let-7c, precursor let-7c was transfected into A549 cells. Let-7c down-regulated IV M1 expression at both the (+) cRNA and protein levels. Furthermore, transfection with a let-7c inhibitor enhanced the expression of M1. Therefore, let-7c may reduce IV replication by degrading M1 (+) cRNA. This is the first report indicating that cellular miRNA regulates IV replication through the degradation of viral gene (+) cRNA by matching the 3'-UTR of the viral cRNA. These findings suggest that let-7c plays a role in protecting host cells from the virus in addition to its known cellular functions. 相似文献
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Specific enrichment of miRNAs in Arabidopsis thaliana infected with Tobacco mosaic virus. 总被引:2,自引:0,他引:2
Yuko Tagami Naoko Inaba Natsumaro Kutsuna Yukio Kurihara Yuichiro Watanabe 《DNA research》2007,14(5):227-233
RNA silencing is a broadly conserved machinery and is involved in many biological events. Small RNAs are key molecules in RNA silencing pathway that guide sequence-specific gene regulations and chromatin modifications. The silencing machinery works as an anti-viral defense in virus-infected plants. It is generally accepted that virus-specific small interfering (si) RNAs bind to the viral genome and trigger its cleavage. Previously, we have cloned and obtained sequences of small RNAs from Arabidopsis thaliana infected or uninfected with crucifer Tobacco mosaic virus. MicroRNAs (miRNAs) accumulated to a higher percentage of total small RNAs in the virus-infected plants. This was partly because the viral replication protein binds to the miRNA/miRNA* duplexes. In the present study, we mapped the sequences of small RNAs other than virus-derived siRNAs to the Arabidopsis genome and assigned each small RNA. It was demonstrated that only miRNAs increased as a result of viral infection. Furthermore, some newly identified miRNAs and miRNA candidates were found from the virus-infected plants despite a limited number of examined sequences. We propose that it is advantageous to use virus-infected plants as a source for cloning and identifying new miRNAs. 相似文献
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Laurent Houzet Zachary Klase Man Lung Yeung Annie Wu Shu-Yun Le Mariam Qui?ones Kuan-Teh Jeang 《Nucleic acids research》2012,40(22):11684-11696
MicroRNAs (miRNAs) are 22-nt non-coding RNAs involved in the regulation of cellular gene
expression and potential cellular defense against viral infection. Using in
silico analyses, we predicted target sites for 22 human miRNAs in the HIV
genome. Transfection experiments using synthetic miRNAs showed that five of these miRNAs
capably decreased HIV replication. Using one of these five miRNAs, human miR-326 as an
example, we demonstrated that the degree of complementarity between the predicted viral
sequence and cellular miR-326 correlates, in a Dicer-dependent manner, with the potency of
miRNA-mediated restriction of viral replication. Antagomirs to miR-326 that knocked down
this cell endogenous miRNA increased HIV-1 replication in cells, suggesting that miR-326
is physiologically functional in moderating HIV-1 replication in human cells. 相似文献