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BSEは人間から牛に感染した?[news at nature.com]
http://www.asyura2.com/0505/gm11/msg/328.html
投稿者 ネオファイト 日時 2005 年 9 月 02 日 23:57:58: ihQQ4EJsQUa/w
 

2名のイギリス人研究者コルチェスター父娘は、これまで羊のスクレイピーが牛に感染したと考えられているBSE起源説に対して、人間の異常プリオンが牛に感染したのではないかと言う仮説を立て、ランセットに発表した。

イギリスでは60から70年代にバングラディシュから家畜の骨を輸入して肉骨粉にしていたが、その後急に狂牛病が現れたのは以前からの肉骨粉とバングラディシュの肉骨粉が異なるからではないかと言う可能性がありうる。バングラディシュではガンジス川に(理想的には火葬後にだが徹底されないまま)死者を流す葬儀の方法がとられているのだが、そのことを考えると、死体から出たプリオンを含んだ川の水が家畜に飲まされて感染してしまったのではないかという仮説がたてられた。しかし、これまでの実験では人間のCJD異常プリオンはネズミには感染しないと言う結果になっている。

【他の英語メディアの報道が詳しいようなところがありますが、論文への参照が書かれていて、時間が経つと有料になってしまうネイチャーニュースを転載。
http://www.guardian.co.uk/uklatest/story/0,1271,-5250003,00.html
http://www.guardian.co.uk/india/story/0,12559,1561293,00.html
http://www.usatoday.com/tech/science/discoveries/2005-09-01-mad-cow-theory_x.htm
http://news.bbc.co.uk/2/hi/science/nature/4201072.stm
例えばBBC記事では人骨そのものが資源として貿易されていたとある。】

http://www.nature.com/news/2005/050829/full/050829-17.html
Published online: 1 September 2005; | doi:10.1038/news050829-17
British duo probes origin of mad cow disease
Did human remains in food spawn the infection in cattle?
Roxanne Khamsi

Human remains in cattle feed could have caused the first case of mad cow disease, two UK researchers propose. The hypothesis seeks to answer lingering questions about the fatal infection, which has affected 180,000 cows in Britain alone since the mid-1980s, and has gone on to cause more than 100 deaths in humans.

Alan Colchester of the University of Kent and his daughter Nancy Colchester, of the University of Edinburgh, point out that during the 1960s and 1970s Britain imported hundreds of thousands of tonnes of whole and crushed bones and animal carcasses. These were used for fertilizer and to feed livestock.

Nearly 50% of these imports came from Bangladesh, where peasants gathering animal materials may have also picked up human remains, the researchers say.

Other experts in the field view the idea with scepticism, saying that proof remains circumstantial. "The argument isn't very compelling because there's no smoking gun evidence," says Surachai Supattapone, an expert in infectious diseases at Dartmouth Medical School in Hanover, New Hampshire.

Sudden appearance

Transmissible spongiform encephalopathies (TSEs) are a group of fatal neurodegenerative diseases that affect mammals. Yet until 1986 no such illness had been spotted in cattle.

Once recognized, bovine spongiform encephalopathy (BSE) became widely known as 'mad cow disease'. The incidence of the disease then rocketed, peaking in late 1992.

Tests indicated misshapen prion proteins in the brains of the cows as the source of the problem. And when authorities banned the practice of recycling animal remains into cattle feed the number of sick livestock began to drop.

But experts continue to puzzle over how BSE arose in the first place.

Sporadic source

One of the most widely believed theories is that prions responsible for sheep scrapie got incorporated into cattle feed. Scientists argue that ingested scrapie prions radically altered the normal, analogous proteins in one cow, which then developed the first case of BSE.

But the Colchesters point out that cows have been exposed to scrapie for 70 years, so it is hard to explain why BSE emerged only recently.

They propose that a more likely source is recent exposure to human remains carrying sporadic Creutzfeldt-Jakob Disease (CJD), a TSE thought to arise spontaneously in people.

Religious customs in Bangladesh and surrounding areas mean that many corpses are disposed of in rivers. People may have collected remnants from such bodies when foraging for animal carcasses, the Colchesters argue in The Lancet[1]. Any prions in these corpses might then have caused mad cow disease.

Experts agree that the theory needs to be checked. More information needs to be collected, they say, about the number of deaths from CJD in the Indian subcontinent, what happened to the bodies, and whether prions could have been transmitted in the way proposed. When human sporadic CJD prions were injected into mice in previous studies, the mice did not become ill[2].

References

1. Colchester A. & Colchester N. et al. Lancet, 366. 856 - 861 (2005).
2. Scott M . R., Peretz D., Nguyen H. O., Dearmond S. J. & Prusiner S. B. J. Virol., 79. 5259 - 5271 (2005). | http://chemport.cas.org/cgi-bin/sdcgi?APP=ftslink&action=reflink&origin=npg&version=1.0&coi=1:CAS:528:DC%2BD2MXjs12qt7s%3D&pissn=&pyear=2005&md5=60602739807e37690cc83841e3fdf0b1 ChemPort |

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