Warning of second wave of vCJD

LONDON - The prospect of the human form of mad-cow disease becoming an epidemic evolving over decades cannot be ruled out, according to a medical expert.

A team of scientists based at Imperial College, London, has uncovered data which has given experts a greater understanding of the potential risks posed by variant Creutzfeldt-Jakob Disease.

The research has revealed that those patients so far seen with vCJD - which attacks the brain causing death - may be genetically disposed to have the shortest "incubation" periods.

Scientists believe that there may be differing degrees of vulnerability to prion diseases like vCJD in those who have the genetic type susceptible to the killer condition.

The first cases of vCJD were detected in March, 1996, and heath experts concluded that the most likely origin of the disease was from eating BSE-infected cattle.

Professor John Collinge, director of the Medical Research Council Prion Unit, led the research which confirms that a number of genes are involved in susceptibility to prion disease in mice.

Mouse and human genomes are similar, so researchers believe that it is almost certain they will find corresponding genes in humans which have the same role to play.

Collinge said: "Three genetic types referred to as MM, VV and MV are seen in the population.

"All those who have so far developed vCJD were from the MM genotype but we expected to find other genes that would influence susceptibility."

He added: "Prion diseases develop over a quite different time-scale and we cannot rule out an epidemic that evolves over decades."

The findings would mean that the current cases are just the tip of the iceberg and that a "second wave" of cases will emerge.

According to the latest figures from the British Department of Health, 99 cases of vCJD have been recorded to date.

But it remains unclear how many other people have been exposed to BSE and what proportion of these will eventually develop the human form of the disease.

Prions cause fatal degenerative brain diseases. As with conditions like cancer and heart disease, genetic factors are thought to be involved in determining an individual's risk of developing CJD, after exposure to the infective agent.

All patients identified so far have a particular variation in their genetic make-up (MM), shared by about 40 per cent of white Britons.

The current estimates assume that only people with the MM genetic make-up will contract the disease if they come into contact with the infective agent, for example by eating contaminated meat.

However, Collinge warns that such predictions may be "overly optimistic."

"This study reminds us that we cannot be complacent about the potential risks to public health posed by BSE."

"We cannot rule out an epidemic that evolves over decades."

- AGENCIES