More than 6 million Australians living with liver disease may benefit from a world-first discovery from the Westmead Institute that will help predict risk of the disease, enabling life-saving early intervention.<\/p>\n The international team, led by Professor Jacob George and Doctor Mohammed Eslam, has shown that variations in the interferon lambda 3 (INLF3) protein are responsible for tissue damage in the liver.<\/p>\n Lead author of the study, Professor Jacob George, said this significant outcome will help to predict risk of liver disease in individuals and allow early lifestyle changes to control risk factors such as obesity and type II diabetes.<\/p>\n \u201cThis important discovery will play a vital role in reducing the burden of liver disease, which is now the fifth most common cause of death in Australia and costs more than $50 billion each year.<\/p>\n \u201cOur team has designed a diagnostic tool based on our discoveries, which is freely available for all doctors to use, to help predict liver fibrosis risk.<\/p>\n \u201cThis test will help to determine whether an individual is at high risk of developing liver fibrosis, or whether a patient\u2019s liver disease will progress quickly or slowly, based on their genetic makeup.<\/p>\n \u201cThis is important, because simple and early interventions will extend and significantly improve the quality of life for patients and may reduce their need for treatment,\u201d Professor George said.<\/p>\n \u201cOur results show that it is possible to develop new targeted treatments for liver fibrosis and possibly even scarring in other organs such as the heart, lung and kidneys.\u201d<\/p><\/blockquote>\n <\/p>\n <\/p>\n The research team had previously identified that the common genetic variations associated with liver fibrosis were located on chromosome 19 between the IFNL3 and IFNL4 genes.<\/p>\n Building on this research in their latest study, the team analysed liver samples from 2000 patients with Hepatitis C, using state-of-the art genetic and functional analysis, to determine the specific IFNL protein responsible for liver fibrosis.<\/p>\n The research, which is published in the prestigious\u00a0Nature Genetics<\/em>\u00a0journal, demonstrated that following injury there is increased migration of inflammatory cells from blood to the liver, increasing IFNL3 secretion and liver damage.<\/p>\n Notably, this response is determined to a great extent by an individual\u2019s inherited genetic makeup.<\/p>\n Co-lead author, Doctor Mohammed Eslam, said this discovery holds great promise for the development of effective therapeutic treatments for liver disease.<\/p>\n \u201cThere is an urgent need for a safe medicines that can stop the progression of liver damage. There is currently no treatment available for patients with advanced fibrosis, and liver transplantation is the only treatment for liver failure.<\/p>\n \u201cNow that we\u2019ve identified IFNL3 as the cause of liver scarring, we can work towards developing new treatments specifically targeting this gene.<\/p>\n \u201cThis could be medicine targeting IFNL3 that is tailored to an individual\u2019s genetic makeup, but could also include modifying usual treatment depending on whether a patient has IFNL3 risk genes.<\/p>\n \u201cOur results show that it is possible to develop new targeted treatments for liver fibrosis and possibly even scarring in other organs such as the heart, lung and kidneys,”\u00a0Dr Mohammed concluded.<\/p>\n The research team will now extend their work to further understand the fundamental mechanisms of how IFNL3 contributes to liver disease progression and to translate these discoveries into new therapeutic treatments.<\/p>\n![\"\"](\"\/wp-content\/uploads\/2024\/09\/Professor-Jacob-George-and-Dr-Mohammed-Eslam.jpg\")