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World J Gastroenterol. Nov 7, 2013; 19(41): 7055-7061
Published online Nov 7, 2013. doi: 10.3748/wjg.v19.i41.7055
Published online Nov 7, 2013. doi: 10.3748/wjg.v19.i41.7055
Interaction of IFNL3 with insulin resistance, steatosis and lipid metabolism in chronic hepatitis C virus infection
Mohammed Eslam, Jacob George, Golo Ahlenstiel, Storr Liver Unit, Westmead Millennium Institute and Westmead Hospital, University of Sydney, Sydney, NSW 2145, Australia
David R Booth, Institute for Immunology and Allergy Research, Westmead Millennium Institute, University of Sydney, Sydney, NSW 2145, Australia
Author contributions: Eslam M and Ahlenstiel G designed and wrote the manuscript and created the tables; Booth DR and George J contributed to the writing and revised the manuscript.
Supported by A National Health and Medical Research Council Project grant, APP1006759 and the Robert W. Storr bequest to the Sydney Medical Foundation of the University of Sydney, to Ahlenstiel G and George J; an International Postgraduate Research Scholarships and an Australian Postgraduate Award of the University of Sydney, to Eslam M
Correspondence to: Dr. Golo Ahlenstiel, Storr Liver Unit, Westmead Millennium Institute and Westmead Hospital, University of Sydney, Sydney, NSW 2145, Australia. golo.ahlenstiel@sydney.edu.au
Telephone: +61-2-98457705 Fax: +61-2-96357582
Received: July 27, 2013
Revised: September 14, 2013
Accepted: September 29, 2013
Published online: November 7, 2013
Processing time: 112 Days and 1.6 Hours
Revised: September 14, 2013
Accepted: September 29, 2013
Published online: November 7, 2013
Processing time: 112 Days and 1.6 Hours
Core Tip
Core tip: Metabolic changes are inextricably linked to chronic hepatitis C (CHC). Recently polymorphisms in the IFNL3 region have been shown to be strongly associated with spontaneous and treatment induced recovery from hepatitis C virus (HCV) infection. Further, circumstantial evidence suggests a link between IFNL3 single nucleotide polymorphisms and lipid metabolism, steatosis and insulin resistance in CHC. The emerging picture suggests that the responder genotypes of IFNL3 polymorphisms are associated with a higher serum lipid profile, and less frequent steatosis and insulin resistance. This review analyzes the current data regarding this interaction and its meaning for HCV pathogenesis and disease progression.