Abstract
Epstein-Barr virus (EBV) or human herpesvirus 4 (HHV-4) is a ubiquitous human oncogenic virus, and the first human virus found to express microRNAs (miRNAs). Its genome contains two regions encoding more than 40 miRNAs that regulate expression of both viral and human genes. There are numerous evidences that EBV miRNAs impact immune response, affect antigen presentation and recognition, change T- and B-cell communication, drive antibody production during infection, and have a role in cell apoptosis. Moreover, the ability of EBV to induce B-cell transformation and take part in mechanisms of oncogenesis in humans is well known. Although EBV infection is associated with development of various diseases, the role of its miRNAs is still not understood. There is abundant data describing EBV miRNAs in nasopharyngeal carcinoma and several studies that have tried to evaluate their role in gastric carcinoma and lymphoma. This review aims to summarize so far known data about the role of EBV miRNAs in altered regulation of gene expression in human cells in EBV-associated diseases.
Highlights
Epstein-Barr virus (EBV) or human herpesvirus 4 (HHV-4) is a ubiquitous human oncogenic virus that belongs to the family Herpesviridae, subfamily Gammaherpesvirinae, and genus Lymphocryptovirus [1].Since its first description in 1964 and subsequent recognition of its ability to induce B-cell transformation in vitro, EBV has been extensively used as a model for research focusing on fundamental mechanisms of oncogenesis in humans
Latent infection with EBV may be associated with development of various malignancies originating from epithelial cells, lymphocytes, and mesenchymal cells, including posttransplant B-cell lymphomas, Hodgkin’s and non-Hodgkin’s lymphomas, diffuse large B-cell lymphoma, Burkitt’s lymphoma, natural killer (NK)/T-cell lymphoma, nasopharyngeal carcinoma (NPC), and gastric carcinoma (GC) [7,8]
Wong et al (2018) showed that miR-BART7 reduces the expression of transforming growth factor β-1 (TGF-β1) in NPC cells and impairs the NK-cell-mediated recognition of virus-infected cells [33] (Figure 2)
Summary
Epstein-Barr virus (EBV) or human herpesvirus 4 (HHV-4) is a ubiquitous human oncogenic virus that belongs to the family Herpesviridae, subfamily Gammaherpesvirinae, and genus Lymphocryptovirus [1]. Since its first description in 1964 and subsequent recognition of its ability to induce B-cell transformation in vitro, EBV has been extensively used as a model for research focusing on fundamental mechanisms of oncogenesis in humans. EBV-encoded cellular mRNAs in infected cells, extending their role beyond regulating various stages of the EBV miRNAs (EBV miRNAs) target both viral and cellular mRNAs in infected cells, extending their role replication cycle. They influence cellular proliferation and apoptosis and play a part in driving beyond regulating various stages of the EBV replication cycle They influence cellular proliferation and diverse molecular pathways of oncogenesis and evading innate and adaptive immune responses. The apoptosis and play a part in driving diverse molecular pathways of oncogenesis and evading innate aim of this review is to summarize current views on the role of EBV miRNAs in altered gene and adaptive immune responses. EBV miRNAs in altered gene expression associated with immune evasion and tumorigenesis
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