An Update on the Metabolic Landscape of Oncogenic Viruses

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.

Serum ApoB/ApoA1 ratio in patients with CHB and the occurrence of HBV related cirrhosis and HBV related hepatocellular carcinoma

“…Epigenetic silencing of ApoA1 gene expression by CpG island DNA hypermethylation induced by HBV can also reduce serum ApoA1 level 39 . HBV suppresses ApoB production by inhibiting microsomal triglyceride transfer protein expression 24 , overexpression of HBx leads to negative regulation of microsomal TG transfer proteins, which can increase the expression of β-d-mannoside-1, 4-N-acetylglucosaminyl transferase-III, and cause inhibition of ApoB secretion and intracellular accumulation of TG and TCh 40 .…”

Epstein–Barr Virus Latent Membrane Protein 2A (LMP2A) Enhances ATP Production in B Cell Tumors through mTOR and HIF-1α

“…For many oncogenic viruses, oncogenic transformation occurs years later and via numerous mechanisms. However, one requirement for all of these processes is the need to modify metabolism so that uncontrolled proliferation and survival can occur [40]. While viruses have developed many pathways to alter metabolisms, almost all oncogenic viruses increase HIF-1α levels via multiple pathways [41].…”