It has been known for a number of years that the ability of some people to spontaneously combat infection with hepatitis C (HCV) – and respond to treatment – is genetically determined. This ability is due to genetic differences in the part of the genome that contains lambda interferons (IFN?). Until now, however, nobody has known what these genetic differences mean.

A new interferon called IFN?4 was found in humans in early 2013. It turned out that the people who produce IFN?4 do not recover from HCV infection very well. What researchers did not know, however, was how this new interferon worked, and they were thereby unable to determine why it is harmful during HCV infection.

An international team led by researchers at Aarhus University therefore decided to find out how this interferon works. As the first in the world, they succeeded in culturing and purifying IFN?4, thereby gaining a unique opportunity to shed light on how this protein functions.

Their experiments showed that IFN?4 worked just as well as the other members of the IFN? family, and that they signalled the same way. However, there was a difference in the way IFN?4 was produced. While the other members of the IFN? family were released from the cells in large numbers, only a small amount of IFN?4 left the cells.

Even though the researchers thus came a long way in finding the answer to why people with IFN?4 do not recover well from HCV infection, their future experiments will now be targeted towards clarifying whether this difference in secretion can explain why they are poor at producing IFN?4 during HCV infection. By culturing and purifying IFN?4, however, the researchers have already made enormous progress.

Possible clinical application

Because IFN?4 is connected with a poor response to HCV, medicine aimed at IFN?4 is an obvious goal in the future. This could possibly stop the negative effect of IFN?4, enabling greater success in treating patients with HCV than the forms of treatment currently available.