Abstract
Latent Epstein-Barr virus (EBV) infection is an etiological factor in the progression of several human epithelial malignancies such as nasopharyngeal carcinoma (NPC) and a subset of gastric carcinoma. Reports have shown that EBV produces several viral oncoproteins, yet their pathological roles in carcinogenesis are not fully elucidated. Studies on the recently discovered of EBV-encoded microRNAs (ebv-miRNAs) showed that these small molecules function as post-transcriptional gene regulators and may play a role in the carcinogenesis process. In NPC and EBV positive gastric carcinoma (EBVaGC), 22 viral miRNAs which are located in the long alternative splicing EBV transcripts, named BamH1 A rightward transcripts (BARTs), are abundantly expressed. The importance of several miR-BARTs in carcinogenesis has recently been demonstrated. These novel findings enhance our understanding of the oncogenic properties of EBV and may lead to a more effective design of therapeutic regimens to combat EBV-associated malignancies. This article will review the pathological roles of miR-BARTs in modulating the expression of cancer-related genes in both host and viral genomes. The expression of other small non-coding RNAs in NPC and the expression pattern of miR-BARTs in rare EBV-associated epithelial cancers will also be discussed.
Highlights
The Epstein-Barr virus (EBV) is a ubiquitous gamma herpesvirus that was originally identified in Burkitt’s lymphoma (BL) by Tony Epstein and his colleagues in 1964 [1]
We further demonstrated that EBER1 and its derived small fragments do not bind to Argonaute2 (Ago2), an integral part in the functional RNA-induced silencing complex (RISC) complex (Figure S1B)
To further analyze the variation pattern of EBV strains from 14 normal controls and 31 nasopharyngeal carcinoma (NPC) patients in our population, we showed that the variant distribution of EBV strain was highly similar between NPC
Summary
The Epstein-Barr virus (EBV) is a ubiquitous gamma herpesvirus that was originally identified in Burkitt’s lymphoma (BL) by Tony Epstein and his colleagues in 1964 [1]. It is the first virus known to play an essential role in the induction of human malignancies [2]. EBV infection is common among most population groups worldwide. The virus will not be entirely eliminated and will establish life-long latent infection within memory B cell pool, in which the viral genome circulates as episome and undergoes replication using host cellular expression machinery [4,5]. Latent EBV infection is associated with a wide range of human lymphoid and epithelial malignancies, including
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