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dc.contributor.authorMasson, JJ
dc.contributor.authorBillings, HW
dc.contributor.authorPalmer, CS
dc.date.accessioned2020-12-21T01:53:28Z
dc.date.available2020-12-21T01:53:28Z
dc.date.issued2017-08
dc.identifier.citationMasson, J. J., Billings, H. W. & Palmer, C. S. (2017). Metabolic reprogramming during hepatitis B disease progression offers novel diagnostic and therapeutic opportunities.. Antivir Chem Chemother, 25 (2), pp.53-57. https://doi.org/10.1177/2040206617701372.
dc.identifier.issn0956-3202
dc.identifier.urihttp://hdl.handle.net/11343/256702
dc.description.abstractMetabolic 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.
dc.languageeng
dc.publisherSAGE Publications
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0
dc.titleMetabolic reprogramming during hepatitis B disease progression offers novel diagnostic and therapeutic opportunities.
dc.typeJournal Article
dc.identifier.doi10.1177/2040206617701372
melbourne.affiliation.departmentMicrobiology and Immunology
melbourne.source.titleAntiviral Chemistry and Chemotherapy
melbourne.source.volume25
melbourne.source.issue2
melbourne.source.pages53-57
dc.rights.licenseCC BY-NC
melbourne.elementsid1228949
melbourne.openaccess.pmchttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC5890528
melbourne.contributor.authorPalmer, Clovis
dc.identifier.eissn2040-2066
melbourne.accessrightsOpen Access


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