Loss of function of the new interferon IFN-λ4 may confer protection from hepatitis C.
Attempts to elucidate the mechanism underpinning the genetic association between IFNL3, previously called IL28B, and clearance of hepatitis C virus have, by and large, been unsuccessful. A study in this issue suggests that a new gene, IFNL4, may be responsible.
Institute for Immunology and Allergy Research, Westmead Millennium Institute, University of Sydney, Sydney, New South Wales, Australia. jacob.george@sydney.edu.au
David
D
Booth
Jacob
J
George
D056945:Hep G2 Cells; D006526:Hepatitis C / Q000276:immunology / Q000517:prevention & control*; D006801:Humans; D007378:Interleukins / Q000235:genetics* / Q000276:immunology; D015810:Linkage Disequilibrium; D008954:Models, Biological; D010766:Phosphorylation; D011110:Polymorphism, Genetic / Q000235:genetics*; D050794:STAT1 Transcription Factor / Q000378:metabolism; D050795:STAT2 Transcription Factor / Q000378:metabolism; D013045:Species Specificity
D007378:Interleukins; D050794:STAT1 Transcription Factor; D050795:STAT2 Transcription Factor