Metabolic reprogramming during hepatitis B disease progression offers novel diagnostic and therapeutic opportunities - PubMed (original) (raw)
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Metabolic reprogramming during hepatitis B disease progression offers novel diagnostic and therapeutic opportunities
Jesse Jr Masson et al. Antivir Chem Chemother. 2017 Aug.
Abstract
Metabolic remodeling occurs in immune cells during an infection. Host cells must upregulate energy production for growth, proliferation, and effector functions to limit the damage imposed by pathogens. One example, the hepatitis B virus, induces hepatic injury in human hepatocytes through dysregulation of aerobic glycolysis and lipid metabolism. Increased glycolytic metabolism mediated by elevated expression of Glut1, glucose influx, and lactate secretion is associated with this Warburg phenotype, a classic metabolic signature also observed in cancer cells. This article brings into focus the tight interaction between HBV infection and metabolic dysfunction and how these processes facilitate the progression of end-stage liver diseases, such as hepatocellular carcinoma. We also provide evidence and models by which other viruses such as HIV and Zika disrupt their host metabolic machinery. The emergence of the immunometabolism field provides novel opportunities to take advantage of intermediary metabolites and key metabolic pathways for diagnostic and therapeutic purposes.
Keywords: HIV; Hepatitis B virus; hepatitis C virus; immunotherapy.
Conflict of interest statement
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Figures
Figure 1.
A model proposing mechanisms by which hepatitis B virus dysregulates glucose and lipid metabolism in infected liver. Hepatitis B virus X protein (HBx) causes metabolic reprogramming and cellular damage. Abnormal lipid accumulation and increased glucose uptake by cancer cells may drive end-stage liver diseases and HCC. HCC: hepatocellular carcinoma.
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