Targeting Metabolic Vulnerabilities in Epstein–Barr Virus-Driven Proliferative Diseases

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Targeting Metabolic Vulnerabilities in Epstein–Barr Virus-Driven Proliferative Diseases
Title:
Targeting Metabolic Vulnerabilities in Epstein–Barr Virus-Driven Proliferative Diseases
Journal Title:
Cancers
Publication Date:
30 June 2023
Citation:
Leung, N. Y. T., & Wang, L. W. (2023). Targeting Metabolic Vulnerabilities in Epstein–Barr Virus-Driven Proliferative Diseases. Cancers, 15(13), 3412. https://doi.org/10.3390/cancers15133412
Abstract:
The metabolism of cancer cells and Epstein–Barr virus (EBV) infected cells have remarkable similarities. Cancer cells frequently reprogram metabolic pathways to augment their ability to support abnormal rates of proliferation and promote intra-organismal spread through metastatic invasion. On the other hand, EBV is also capable of manipulating host cell metabolism to enable sustained growth and division during latency as well as intra- and inter-individual transmission during lytic replication. It comes as no surprise that EBV, the first oncogenic virus to be described in humans, is a key driver for a significant fraction of human malignancies in the world (~1% of all cancers), both in terms of new diagnoses and attributable deaths each year. Understanding the contributions of metabolic pathways that underpin transformation and virus replication will be important for delineating new therapeutic targets and designing nutritional interventions to reduce disease burden. In this review, we summarise research hitherto conducted on the means and impact of various metabolic changes induced by EBV and discuss existing and potential treatment options targeting metabolic vulnerabilities in EBV-associated diseases.
License type:
Attribution 4.0 International (CC BY 4.0)
Funding Info:
This research is supported by core funding from: Biomedical Research Council (BMRC)
Grant Reference no. : NA

This research / project is supported by the National Medical Research Council - Open Fund - Young Individual Research Grant
Grant Reference no. : MOH-000545
Description:
ISSN:
2072-6694
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