Interaction of IFNL3 with insulin resistance, steatosis and lipid metabolism in chronic hepatitis C virus infection.
Metabolic changes are inextricably linked to chronic hepatitis C (CHC). Recently polymorphisms in the IFNL3 (IL28B) 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.
Mohammed Eslam, Jacob George, Golo Ahlenstiel, Storr Liver Unit, Westmead Millennium Institute and Westmead Hospital, University of Sydney, Sydney, NSW 2145, Australia.
Mohammed
M
Eslam
David R
DR
Booth
Jacob
J
George
Golo
G
Ahlenstiel
D015415:Biomarkers / Q000097:blood; D018450:Disease Progression; D005234:Fatty Liver / Q000235:genetics* / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D019698:Hepatitis C, Chronic / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000821:virology; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics*; D007372:Interferons; D007378:Interleukins / Q000235:genetics* / Q000378:metabolism; D050356:Lipid Metabolism / Q000235:genetics*; D008055:Lipids / Q000097:blood; D065626:Non-alcoholic Fatty Liver Disease; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D011379:Prognosis; D012307:Risk Factors; D000095022:Interferon Lambda
D015415:Biomarkers; D007372:Interferons; D007378:Interleukins; D008055:Lipids; C000624353:interferon-lambda, human; D000095022:Interferon Lambda
Chronic hepatitis C; IFNL3; Insulin resistance; Lipids