New virus has been developed that can convert cells damaged by toxins into healthy cells
A bespoke virus that targets damaged liver cells and converts them into healthy cells could prevent the need for liver transplants, according to research.
More than 10,000 people in the UK die every year from cirrhosis of the liver, which particularly affects heavy drinkers.
But now, a team of researchers at University College San Francisco have developed a way of converting cells damaged by toxins, called myofibroblasts, into healthy cells, called hepatocytes.
The study’s senior author, Dr Holger Willenbring said: “Part of why this works is that the liver is a naturally regenerative organ, so it can deal with new cells very well.
“What we see is that the converted cells are not only functionally integrated in the liver tissue, but also divide and expand, leading to patches of new liver tissue.”
The process specifically targets liver fibrosis, which is the progressive scarring of the liver and the primary driver of liver disease.
Fibrosis occurs when certain cells in the liver, called hepatocytes, cannot regenerate fast enough to keep up with the damage caused by booze or certain diseases like hepatitis C or fatty liver disease caused by obesity.
When this happens, ‘patches’ are created – similar to fixing a flat tyre – but when too many of these patches appear, the liver begins to fail.
The liver is able to adapt, but when its overall functionality drops below the critical threshold of 20 per cent, patients can often die within two years.
Dr Willenbring said: “Liver fibrosis is not rare. It’s actually the end stage of many chronic liver diseases.
“Obesity, for instance, can lead to fatty liver disease, which is predicted to become the number one cause of liver fibrosis in the next 10 years.”
A team of researchers at Heidelberg University Hospital in Germany, headed by Dr Willenbring, have found a way of converting these ‘patches’ into new, healthy hepatocytes.
Following years of work, the team have identified an adeno-associated virus (AAV) which is able to specifically infect the patches.
They found that by filling the AVV viruses with a fate-changing cocktail, the virus converted the damaged patches into functional liver cells.
The number of new cells were relatively small – often less than 1% – but this was often sufficient to reduce fibrosis and improve liver function.
Dr Willenbring said that although the new technique is nowhere near replacing the current standard of care in liver disease, this technique does offer an exciting development.
He said: “A liver transplant is still the best cure. This is more of a patch.
“But if it can boost liver function by just a couple percent, that can hopefully keep patients’ liver function over that critical threshold, and that could translate to decades more of life.”
The study was published in the journal Cell Stem Cell.