Have scientists found a CURE for alcoholism? New virus can ‘repair the liver damage caused by drinking’
- Scientists have created a bespoke virus which can be sent into liver cells
- It targets damaged cells in the organ and converts them into healthy ones
- Could keep liver functioning longer – allowing patients to live for decades
- A transplant is still the best cure but this is an ‘exciting development’
Madlen Davies for MailOnline
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People with liver disease may soon live for decades longer – as scientists have created a virus that targets damaged cells in the organ and converts them into healthy ones.
More than 100,000 people in the US die every year from chronic liver disease and cirrhosis – where the liver becomes irreparably scarred and stops working.
And cirrhosis – which particularly affects heavy drinkers – kills 10,000 people a year in the UK.
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.
In years to come, the technique could buy patients time – possibly preventing the need for a transplant – and helping them to live for years longer, researchers said.
A bespoke virus that targets damaged liver cells and converts them into healthy cells could repair the damage done by alcohol, scientists from University College San Francisco claim
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 which causes liver disease.
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Fibrosis occurs when certain cells in the liver, called hepatocytes, cannot regenerate fast enough to keep up with the damage caused by alcohol 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.
The process specifically targets liver fibrosis, which is the progressive scarring of the liver which causes liver disease. It could keep the organ working – translating to decades more of life, researchers claim
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.’
Working closely with team of researchers at Heidelberg University Hospital in Germany, Dr Willenbring and his team have found a way of converting these ‘patches’ into new, healthy liver cells.
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 liver cells that were functional.
The number of new cells were relatively small – often less than one per cent – but this was often sufficient to reduce fibrosis and improve liver function.
Dr Willenbring said that the offers 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 per cent, 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.
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