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Abstract
Epstein–Barr virus (EBV) lytic induction therapy is an emerging virus-targeted therapeutic approach that exploits the presence of EBV in tumor cells to confer specific killing effects against EBV-associated malignancies. Efforts have been made in the past years to uncover the mechanisms of EBV latent-lytic switch and discover different classes of chemical compounds that can reactivate the EBV lytic cycle. Despite the growing list of compounds showing potential to be used in the lytic induction therapy, only a few are being tested in clinical trials, with varying degrees of success. This review will summarize the current knowledge on EBV lytic reactivation, the major hurdles of translating the lytic induction therapy into clinical settings, and highlight some potential strategies in the future development of this therapy for EBV-related lymphoid and epithelial malignancies.
Highlights
Epstein–Barr virus (EBV) infects more than 90% of adults worldwide
EBV is associated with lymphomas such as endemic Burkitt lymphoma (BL), Hodgkin lymphoma (HL), T-/NK, and B-cell non-Hodgkin lymphoma as well as epithelial carcinomas, which include undifferentiated nasopharyngeal carcinoma (NPC) and a subset of gastric carcinoma (EBVaGC) [2,3,4]
Induction of hypoxia has been shown to reactivate EBV lytic cycle through the binding of hypoxia-inducible factor 1 (HIF-1) to the hypoxia response element motif on Zp and/or by the activation of the ERK1/2 signaling pathway [35,36]. Iron chelators such as deferoxamine, Dp44mT, and a novel compound known as C7 were found to stabilize HIF-1α, which subsequently leads to the reactivation of EBV lytic cycle [36]
Summary
Epstein–Barr virus (EBV) infects more than 90% of adults worldwide. While its primary infection is often asymptomatic, it can manifest as infectious mononucleosis (IM) in adolescents and young adults [1]. Owing to the limited choice and the low expression of these viral proteins, it is difficult to target EBV-positive tumor cells . The latent virus within the infected cells enters into lytic cycle, in which >70 viral proteins are produced [5]. Owing to the massive number cellular stresses, for example, oxidative stress, hypoxia, autophagy, and inflammation, as wellof asviral proteins expressed during the lytic cycle,micro they RNAs may be potentially for EBV-specific through modulation of host and viral. EBV-positive cells.a few there were many studies in the past decades studying the lytic induction therapy, only. There were many studies in the past decades studying the lytic induction therapy, only a were conducted in the setting of clinical trials.
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