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Metabolic reprogramming during hepatitis B disease progression offers novel diagnostic and therapeutic opportunities.

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.
PMID
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Authors

Mayor MeshTerms

Disease Progression

Keywords

HIV

Hepatitis B virus

hepatitis C virus

immunotherapy

Journal Title antiviral chemistry & chemotherapy
Publication Year Start




PMID- 28768434
OWN - NLM
STAT- MEDLINE
DA  - 20170803
DCOM- 20170811
LR  - 20170811
IS  - 2040-2066 (Electronic)
IS  - 0956-3202 (Linking)
VI  - 25
IP  - 2
DP  - 2017 Aug
TI  - Metabolic reprogramming during hepatitis B disease progression offers novel
      diagnostic and therapeutic opportunities.
PG  - 53-57
LID - 10.1177/2040206617701372 [doi]
AB  - 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.
FAU - Masson, Jesse Jr
AU  - Masson JJ
AD  - 1 Centre for Biomedical Research, Burnet Institute, Melbourne, Australia.
FAU - Billings, Hugh Ww
AU  - Billings HW
AD  - 1 Centre for Biomedical Research, Burnet Institute, Melbourne, Australia.
FAU - Palmer, Clovis S
AU  - Palmer CS
AD  - 1 Centre for Biomedical Research, Burnet Institute, Melbourne, Australia.
AD  - 2 Department of Infectious Diseases, Monash University, Melbourne, Australia.
AD  - 3 Department of Microbiology and Immunology, University of, Melbourne, Melbourne,
      Australia.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Antivir Chem Chemother
JT  - Antiviral chemistry & chemotherapy
JID - 9009212
SB  - IM
MH  - Carcinoma, Hepatocellular/complications/prevention & control/virology
MH  - *Disease Progression
MH  - Hepatitis B/diagnosis/drug therapy/immunology/*metabolism
MH  - Hepatitis B virus/drug effects/immunology/physiology
MH  - Humans
MH  - Liver Diseases/complications
MH  - Molecular Targeted Therapy
OTO - NOTNLM
OT  - HIV
OT  - Hepatitis B virus
OT  - hepatitis C virus
OT  - immunotherapy
EDAT- 2017/08/05 06:00
MHDA- 2017/08/12 06:00
CRDT- 2017/08/04 06:00
AID - 10.1177/2040206617701372 [doi]
PST - ppublish
SO  - Antivir Chem Chemother. 2017 Aug;25(2):53-57. doi: 10.1177/2040206617701372.