Somewhere along our evolutionary path, we lost the ability to defend against hepatitis C. But not all humans lost this ability.
The hepatitis C virus (HCV) infects around 1% of the human population and is a devastating pathogen. In most people, it silently infects the liver for decades, often causing life-threatening inflammation, scarring and even cancer. How the virus achieves this feat has long puzzled scientists.
In our latest study, published in PLOS Pathogens, we found that a molecule that defends against HCV and other pathogens is weaker in humans than in our closest relative, the chimpanzee. This weakened molecule might have made it easier for some viruses, such as HCV, to infect humans and cause disease.
We are not defenceless against HCV. Our liver responds to infection by producing antiviral molecules called interferons. You can think of these molecules as the antiviral alarm system. Interferons are made rapidly once an invader has been spotted inside a cell. They are then released by the infected cell where they float across the nearby cells, warning them that a virus is near and forcing them to defend themselves by making hundreds more antiviral molecules.
In particular, we produce what is known as “lambda” – interferons against HCV that work well in liver cells. Strangely, one interferon lambda, called IFNL4, is associated with a reduced chance of clearing HCV, making it easier for the virus to silently infect the liver for decades. How an antiviral molecule appears to help a virus to sustain infection over such a long time, and how this may have evolved, remains a mystery.
|Read on: Not all people are equally vulnerable to hepatitis C|