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Abstract
The Epstein-Barr virus (EBV) is known as an oncogenic herpesvirus that has been implicated in the pathogenesis of various malignancies. EBV-encoded RNAs (EBERs) are non-coding RNAs expressed abundantly in latently EBV-infected cells. Herein, I summarize the current understanding of the functions of EBERs, including the interactions with cellular factors through which EBERs contribute to EBV-mediated pathogenesis. Previous studies have demonstrated that EBERs are responsible for malignant phenotypes in lymphoid cells, and can induce several cytokines that can promote the growth of various EBV-infected cancer cells. EBERs were also found to bind retinoic acid-inducible gene I (RIG-I) and thus activate its downstream signaling. Furthermore, EBERs induce interleukin-10, an autocrine growth factor for Burkitt’s lymphoma cells, by activating RIG-I/interferon regulatory factor 3 pathway, suggesting that EBER-mediated innate immune signaling modulation contributes to EBV-mediated oncogenesis. Recently, EBV-infected cells were reported to secret EBERs, which were then recognized by toll-like receptor 3 (TLR3), leading to the induction of type I interferon and inflammatory cytokines, and subsequent immune activation. Furthermore, EBER1 was detected in the sera of patients with active EBV-infectious diseases, suggesting that EBER1-meidated TLR3 signaling activation could account for the pathogenesis of active EBV-infectious diseases.
Highlights
Epstein-Barr virus (EBV), a ubiquitous human herpes virus that has infected more than 90% of the global populations, is associated with a variety of malignancies, including endemic Burkitt’s lymphoma (BL), Hodgkin’s lymphoma, nasopharyngeal carcinoma (NPC), gastric carcinoma (GC), and opportunistic lymphoma
EBV-encoded RNAs (EBERs) can be used as target molecules for the in situ hybridization (ISH) detection of EBV-infected cells in tissues [5] and are considered a reliable marker of the presence of EBV, as they are abundantly expressed in latently EBV-infected cells
Iwakiri et al [10,11] demonstrated that EBERs induce insulin-like growth factor-1 (IGF1), which acts as an autocrine growth factor for NPC and GC cells
Summary
Epstein-Barr virus (EBV), a ubiquitous human herpes virus that has infected more than 90% of the global populations, is associated with a variety of malignancies, including endemic Burkitt’s lymphoma (BL), Hodgkin’s lymphoma, nasopharyngeal carcinoma (NPC), gastric carcinoma (GC), and opportunistic lymphoma. These “EBV-associated” cancers are characterized by the proliferation of monoclonal EBV-infected cells with restricted latent viral gene expression [1]. Previous studies have demonstrated the roles of EBERs in EBV oncogenicity. Previous studies have demonstrated that EBERs induce the transcription of various cytokines depending on cell type, such as interleukin-10. Regarding the molecular action mechanisms of EBREs, these ncRNAs were reported to contribute to the EBV infection pathogenesis by modulating of innate immune signals [15,16,17]
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