Describe the aim of this project in 10 words.

To identify the causative protein of the interferon lambda (IFNL3/IFNL4) genetic area associated with inflammation and fibrosis. 

 What have you discovered so far?

Previously we had identified that the common genetic variations associated with liver fibrosis were located on chromosome 19 between the IFNL3 and INFL4 genes.

We have now discovered for the first time that IFNL3 is the protein mediating liver inflammation and fibrosis. This work was published recently in Nature Genetics.

What aspect of this research excites you the most?

Our work fulfils several promises in the era of precision medicine. Firstly, it brings us closer to the goal of personalised medicine. Secondly, we have a better understanding of biology and the way the human body works. And finally, we are a step closer to developing novel potential treatments for liver disease.

How long before your work impacts patient care?

Based on our discoveries, and led by Professor Jacob George, we have designed an online diagnostic tool, which is freely available for all doctors to use to predict liver fibrosis risk. www.fibrogene.com Translating our findings into therapeutics will require some further research.

What is the next step in this line of research?

Our team is working to extend our efforts to further understand the fundamental mechanisms of how IFNL3 contributes to liver disease progression and to translate these discoveries into new therapeutic treatments. This could be medicine targeting IFNL3 that is tailored to an individual’s genetic makeup, but could also involve modifying usual treatment depending on whether a patient has IFNL3 risk genes.

What’s your Holy Grail – the one thing you’d like to achieve in your career?

To help improve health services and ease patients’ suffering.

 Who has inspired you?

My family has influenced a lot of what I’m doing.