LAUSR

Simple Summary Cancer cells amplify in an uncontrolled fashion. The resulting tumor and metastases need to ensure their survival in the body. To achieve this, cancer cells display increased nutritional needs and an altered metabolism. These metabolic changes start to be targeted for therapeutic interventions in the context of a number of different cancers. Similar to cancer, cells infected with viruses that cause cancer, so-called “oncoviruses”, have altered nutritional needs to support the amplification and spread of new progeny viruses and to ensure the survival of infected cells in the host. Here, we give an update on the similarities between the metabolic alterations observed in many types of cancers and those induced by oncogenic viruses. Furthermore, we discuss the antiviral activities of metabolic inhibitors used for the treatment of cancer. Abstract Viruses play an important role in cancer development as about 12% of cancer types are linked to viral infections. Viruses that induce cellular transformation are known as oncoviruses. Although the mechanisms of viral oncogenesis differ between viruses, all oncogenic viruses share the ability to establish persistent chronic infections with no obvious symptoms for years. During these prolonged infections, oncogenic viruses manipulate cell signaling pathways that control cell cycle progression, apoptosis, inflammation, and metabolism. Importantly, it seems that most oncoviruses depend on these changes for their persistence and amplification. Metabolic changes induced by oncoviruses share many common features with cancer metabolism. Indeed, viruses, like proliferating cancer cells, require increased biosynthetic precursors for virion production, need to balance cellular redox homeostasis, and need to ensure host cell survival in a given tissue microenvironment. Thus, like for cancer cells, viral replication and persistence of infected cells frequently depend on metabolic changes. Here, we draw parallels between metabolic changes observed in cancers or induced by oncoviruses, with a focus on pathways involved in the regulation of glucose, lipid, and amino acids. We describe whether and how oncoviruses depend on metabolic changes, with the perspective of targeting them for antiviral and onco-therapeutic approaches in the context of viral infections.