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

SIMPLE SUMMARY: Discovered in 1964, Epstein-Barr virus was the first human cancer-causing virus identified. Cancer cells reprogram metabolic pathways to augment their ability to support abnormal rates of proliferation and promote spread through metastatic invasion. Over the course of an infection, EBV drastically alters the metabolic landscape within its host cell, leading to a variety of downstream effects such as contributing to uncontrolled and upregulated cell growth—a hallmark of cancer. In this review, we will provide a comprehensive overview of research hitherto conducted on the means and impact of various metabolic changes that EBV induces, as well as discuss existing and potential treatment options targeting vulnerabilities in EBV-transformed metabolism. 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.