Gene boosts resistance to human form of mad cow disease

November 14, 2001 Agence France Presse
People who lack a gene involved in immune responses could be three times likelier to contract the human form of mad cow disease, British researchers say.

The gene, DQ7, occurs in 36 percent of the British population and is part of a system that manufactures bits of proteins for the body's defence system against infection.

Research to be published Thursday by John Collinge and others of the Institute of Neurology, University College London, looked at the genetic makeup of 50 patients with variant Creutzfeldt-Jakob Disease (vCJD). Only 12 percent of the patients had the DQ7 gene, which implies that people with the gene have much better protection against vCJD, they say.

The study, which is published by the British science weekly Nature, sheds light on one of vCJD's enduring mysteries.

The known official toll from the disease is 107 cases in Britain, plus three in France and one in Ireland. There is also a suspected case in Japan.

But attempts to calculate whether the disease will cause tens of thousands of deaths or peter out after a toll of a few hundred have foundered on a reef of variables.

Among the unknowns are: how long the disease takes to incubate after infection, and whether there are genetic factors which make a person more resistant or vulnerable to it.

The Collinge team say the gene link has "important implications" for figuring out the molecular pathways of infection and could also throw up new ideas for medicine to prevent or treat vCJD.

vCJD is the name conferred in 1996 to a type of spongiform encephalopathy -- a disease in which a rogue prion protein destroys brain cells, turning the brain progressively more spongy.

Scientists considered it to be a new form of a rare condition, Creutzfeldt-Jakob disease, and linked it to the consumption of meat from cows infected with the bovine form of this ailment.

However, some voices question this mainstream view.

One dissenting view, published in next Saturday's issue of New Scientist, says that bovine spongiform encephalopathy (BSE) is triggered not by rogue prions but by a common soil bacterium called Acinetobacter.

A team led by Alan Ebringer at King's College London discovered unusually highly levels of antibodies against this bug in samples of infected cow brain.

He believes that antibodies mistake brain and nerve tissue for bacteria and home in it, triggering BSE in cows and vCJD, as well as multiple sclerosis, in humans.

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