Scientists have discovered how the notorious Epstein-Barr Virus (EBV) makes some people vulnerable to developing cancer.

Around 90% of British adults are infected with EBV - but most come to no harm.

However, in a small minority of cases the virus helps to trigger cancer.

EBV has been linked to Hodgkin's disease, Burkitt's lymphoma, and nasopharyngeal cancer, as well as certain rare cancers in immunosupressed transplant patients.

Now scientists from Cancer Research UK's Paterson Institute have discovered how the virus acts to increase the risk that cells will divide in the uncontrolled fashion typical of cancer.

They hope the advance could lead to ways of protecting people from the effects of infection or treating patients with EBV-related cancers.

The researchers focused on a gene called p16 which acts as a brake on cell growth and division.

It was already known that EBV was able to inactivate the p16 braking system - but the way it did this was a mystery.

Sabotaged brakes

In the new study, the researchers tested the effects of EBV in human cells called fibroblasts.

They found that the key was a molecule produced by the virus, known as LMP1.

This molecule neutralises the p16 system, either by switching it off, or sabotaging its effectiveness. This leaves cells free to divide in an uncontrolled way, raising the risk of cancer.

The researchers believe LMP1 may also have other, as yet undiscovered, effects that could also contribute to the development of cancer.

Lead researcher Dr Eiji Hara said: 'Epstein-Barr Virus has a number of different cancer-promoting effects and it's important that we get to the bottom of how it works, so we may be able to find ways of treating or protecting people.

'We think we've found the virus's central cancer trigger, but we've still got a way to go in understanding exactly how the trigger works - it looks as if it may have a few more tricks up its sleeve.'

Professor Robert Souhami, director of clinical research for Cancer Research UK, said: 'Around 15-20% of all cancers are caused by viruses, so it's vital that we get a better handle on the role of viral infection.

'By teasing out the details, we should eventually put ourselves in a position where we have improved treatments for viral cancers and perhaps effective methods of prevention.'

The research is published in the Journal of Cell Biology.