Genetic variation within the IFNL4 loci is closely linked to both spontaneous and treatment induced HCV clearance, as well as to development of fibrosis. Interestingly, there is an inverse relationship between HCV clearance and fibrosis, where the allele, which is protective in term of fibrosis, simultaneously prevent HCV clearance. We hypothesize, that IFNL4 act as a master regulator of liver inflammation and thus that the connection between the IFNL4 gene and fibrosis exist across different ethology’s. We are currently building a cohort of 1200 patient patients suffering from one of several different disorders, HBV infection, NAFLD/NASH or HCV, all of which causes liver inflammation and hence liver fibrosis. Fibrosis was determined by liver biopsies in all patients. We plan to test our hypothesis by examining the correlation between the IFNL4 gene and fibrosis in these patients. 

Members of the ODIN network can register via the matchmaking platform www.confluence.odin.au.dk