Epstein-Barr Virus miR-BART6-3p Inhibits the RIG-I Pathway

Lu, Yuanjun; Qin, Zailong; Jia, Weiping; Zheng, Xiang; Lu, Jianhong; Zhang, Xuemei; Wei, Lingyu; Qiu, Ping; Zheng, Ying; Ou, Chunlin; Ye, Qiurong; Wang, Xiong; Li, Guiyuan; Fu, Yuxin; Yan, Qun; Ma, Jian

doi:10.1159/000479749

Cited by 92 publications

(82 citation statements)

References 48 publications

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“…miR-BART6-3p targets the retinoic acid-inducible gene-I (RIG-I) (an intracellular receptor for double-stranded RNA), thereby suppressing host innate immune responses (27). miR-BART20-5p and miR-BART8 target IFN-γ and the signal transducer and activator of transcription 1 (STAT1), respectively, ultimately suppressing cellular immunity against tumor cells (29).…”

Section: Suppression Of Host Innate Immunity By Ebv Mirnasmentioning

confidence: 99%

Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases

et al. 2020

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Epstein-Barr virus (EBV) is an oncogenic human herpes virus that was discovered in 1964. Viral non-coding RNAs, such as BamHI-A rightward fragment-derived microRNAs (BART miRNAs) or BamHI-H rightward fragment 1-derived miRNAs (BHRF1 miRNA) in EBV-infected cells have been recently reported. Host miRNAs are also upregulated upon EBV infection. Viral and host miRNAs are important in maintaining viral infection and evasion of host immunity. Although miRNAs in EBV-infected cells often promote cell proliferation by targeting apoptosis or cell cycle, this review focuses on the regulation of the recognition of the host immune system. This review firstly describes the location and organization of two clusters of viral miRNAs, then describes evasion from host immune surveillance systems by modulating viral gene expression or inhibiting innate and acquired immunity by viral miRNAs as well as host miRNAs. Another topic is the enigmatic depletion of viral miRNAs in several types of EBV-infected tumor cells. Finally, this review introduces the strong correlation of nasopharyngeal cancer cases with a newly identified single nucleotide polymorphism that enhances BART miRNA promoter activity.

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Section: Suppression Of Host Innate Immunity By Ebv Mirnasmentioning

confidence: 99%

Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases

et al. 2020

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“…At the same time, viral miRNAs can also directly interact with host mRNAs to regulate cellular networks that promote persistence, replication, and/or immune evasion (Bruscella et al, 2017;Cullen, 2006). For example, the Epstein-Barr virus (EBV)-encoded miRNA BART6 inhibits the induction of antiviral immune responses by targeting genes of the retinoic acid-inducible gene I (RIG-I) signaling pathway (Lu et al, 2017), while miRNAs derived from the oncogenic human Kaposi's sarcoma-associated 2.3 | Cellular miRNA regulation and functions in defense Cellular (host) miRNAs regulate nearly every signaling pathway inside the cells and they work in concert with transcription factors to control initiation, maintenance, and resolution of cell response to injury and stress (Mendell & Olson, 2012 (Girardi, López, & Pfeffer, 2018;Trobaugh & Klimstra, 2017), which we will not duplicate. We note, however, that it is not always trivial to understand whether the up-or down-regulation of a given miRNA upon infection is driven by a viral or host mechanism.…”

Section: Functional Roles Of Viral Mirnas Inside Cellsmentioning

confidence: 99%

Extracellular RNA in viral–host interactions: Thinking outside the cell

et al. 2019

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Small RNAs and their associated RNA interference (RNAi) pathways underpin diverse mechanisms of gene regulation and genome defense across all three kingdoms of life and are integral to virus–host interactions. In plants, fungi and many animals, an ancestral RNAi pathway exists as a host defense mechanism whereby viral double‐stranded RNA is processed to small RNAs that enable recognition and degradation of the virus. While this antiviral RNAi pathway is not generally thought to be present in mammals, other RNAi mechanisms can influence infection through both viral‐ and host‐derived small RNAs. Furthermore, a burgeoning body of data suggests that small RNAs in mammals can function in a non‐cell autonomous manner to play various roles in cell‐to‐cell communication and disease through their transport in extracellular vesicles. While vesicular small RNAs have not been proposed as an antiviral defense pathway per se, there is increasing evidence that the export of host‐ or viral‐derived RNAs from infected cells can influence various aspects of the infection process. This review discusses the current knowledge of extracellular RNA functions in viral infection and the technical challenges surrounding this field of research. This article is categorized under: Regulatory RNAs/RNAi/Riboswitches > Regulatory RNAs RNA in Disease and Development > RNA in Disease Regulatory RNAs/RNAi/Riboswitches > RNAi: Mechanisms of Action

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“…Epstein-Barr virus (EBV) is a member of the gamma herpesviruses and was the first confirmed human tumor virus (Ding et al, 2013;Lu et al, 2017). EBV ubiquitously infects more than 90% of the global population and is closely associated with the development of several malignancies, including Burkitt's lymphoma and nasopharyngeal carcinoma (NPC) (Shair et al, 2008;Yu et al, 2012;Young, 2014;Young and Dawson, 2014;Liu et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Epstein-Barr Virus Nuclear Antigen 1 Recruits Cyclophilin A to Facilitate the Replication of Viral DNA Genome

Xin

Liu

et al. 2019

Front. Microbiol.

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Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1)-mediated DNA episomal genome replication and persistence are essential for the viral pathogenesis. Cyclophilin A (CYPA) is upregulated in EBV-associated nasopharyngeal carcinoma (NPC) with unknown roles. In the present approach, cytosolic CYPA was found to be bound with EBNA1 into the nucleus. The amino acid 376-459 of the EBNA1 domain was important for the binding. CYPA depletion attenuated and ectopic CYPA expression improved EBNA1 expression in EBV-positive cells. The loss of viral copy number was also accelerated by CYPA consumption in daughter cells during culture passages. Mechanistically, CYPA mediated the connection of EBNA1 with oriP (origin of EBV DNA replication) and subsequent oriP transcription, which is a key step for the initiation of EBV genome replication. Moreover, CYPA overexpression markedly antagonized the connection of EBNA1 to Ubiquitinspecific protease 7 (USP7), which is a strong host barrier with a role of inhibiting EBV genome replication. The PPIase activity of CYPA was required for the promotion of oriP transcription and antagonism with USP7. The results revealed a strategy that EBV recruited a host factor to counteract the host defense, thus facilitating its own latent genome replication. This study provides a new insight into EBV pathogenesis and potential virus-targeted therapeutics in EBV-associated NPC, in which CYPA is upregulated at all stages.

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Epstein-Barr Virus miR-BART6-3p Inhibits the RIG-I Pathway

Cited by 92 publications

References 48 publications

Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases

Role of Viral and Host microRNAs in Immune Regulation of Epstein-Barr Virus-Associated Diseases

Extracellular RNA in viral–host interactions: Thinking outside the cell

Epstein-Barr Virus Nuclear Antigen 1 Recruits Cyclophilin A to Facilitate the Replication of Viral DNA Genome

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