BSE 'cannot be caught' from infected beef

Humans cannot develop mad cow disease by eating infected beef, according to groundbreaking research by a British scientist due to be published this week.

The experiments, carried out at a London research centre, show that the agent which causes bovine spongiform encephalopathy (BSE) does not react with a human protein that is key to developing the disease. Without this reaction, the disease cannot progress.

The result will come as a huge relief to the beef industry, and to Government ministers and scientists who have insisted that beef is safe to eat amidst mounting public concern. In the past fortnight sales of beef from wholesalers have slumped by 25 per cent, and more than 1,000 schools have removed beef or beef products from their menus.

However, some critics of the Government's stance say they will not change their mind. "There's no way that you can deduce experimentally that it's safe," insists Richard Lacey, Professor of Microbiology at Leeds University.

The new work has been carried out by Professor John Collinge at St Mary's Hospital Medical School, and will be published formally in the science magazine Nature this Thursday.

The Ministry of Agriculture, Fisheries and Food already knows about the results of the work, as it provided some of the funding for it. Ministers and some members of the independent advisory committee on BSE knew the results last week. Professor John Pattison, head of the committee, hinted at "unpublished scientific work" during a press conference last week.

Professor Collinge has consistently refused to discuss his work ahead of publication because Nature imposes an embargo on the authors of papers. His experiment used genetically engineered mice which had been given the human version of a gene called "PrP", which is found in most animals.

PrP is essential to the development of spongiform diseases. The infective agent in the diseases, known as a "prion", causes proteins made by the PrP gene to change shape, causing nerve cells to break apart. This leads to the "spongy" form of diseased brains.

When normal mice with the PrP gene are injected with BSE prions, they develop the disease. Separate work by a Swiss scientist, revealed last week at a London conference, has shown that mice without any PrP gene do not develop disease when injected with BSE.

But when Professor Collinge's genetically engineered mice - in which the mouse PrP gene is replaced with a human one - were injected with BSE- infected material, they did not get the disease. This implies that BSE prions cannot affect the human PrP protein.

The genetic differences between humans and cows appears to form such a high "species barrier" that BSE cannot cross it to cause the brain damage typical of BSE and its human equivalent, Creutzfeldt-Jakob Disease (CJD).

The risks posed by eating beef would therefore be tiny, because injecting infected material into the brain - as was done in these experiments - is thousands of times more effective at causing the disease than feeding it to the animals.

Scientists contacted by the Independent were enthusiastic about the implications of a negative result for public health.

Colin Blakemore, the eminent Oxford neurophysiologist who two weeks ago declared that he would not eat beef, called it "terrifically reassuring".