生物谷報(bào)道：Published online: 11 March 2005; | doi:10.1038/news050307-15
專家爭論是否由天花或者瘟疫有此榮譽(yù),！
中世紀(jì)的歐洲瘟疫的大流行似乎應(yīng)該有意想不到的效果，使10％今天生存下來的人具有可抗HIV的侵染,，但是是什么疾病導(dǎo)致產(chǎn)生抗HIV的免疫性,？研究者認(rèn)為是瘟疫，而反對(duì)者確認(rèn)為是天花,！但清楚的是某些條件促進(jìn)了基因發(fā)生突變幫助產(chǎn)生對(duì)HIV的抗性,。突變產(chǎn)生影響白細(xì)胞表面蛋白CCR5，阻止了HIV進(jìn)入 這些細(xì)胞,，進(jìn)而毀壞免疫系統(tǒng),。
詳細(xì)內(nèi)容參見如下：
Deaths from plague in the Middle Ages may have left more people with a gene that guards against HIV.
Experts argue over whether smallpox or plague should take the credit.
Devastating epidemics that swept Europe during the Middle Ages seem to have had an unexpected benefit - leaving 10% of today's Europeans resistant to HIV infection.
But epidemics of which disease? Researchers claimed this week that plague helped boost our immunity to HIV, but rival teams are arguing that the credit should go to smallpox.
What is clear is that something has boosted the prevalence of a mutation that helps protect against the virus. The mutation, which affects a protein called CCR5 on the surface of white blood cells, prevents HIV from entering these cells and damaging the immune system.
Around 10% of today's Europeans carry the mutation, a significantly higher proportion than in other populations. Why is it so common in Europe? One possibility is that it favours carriers by protecting them from disease. But geneticists know that the mutation, called CCR5-32, appeared some 2,500 years ago - long before HIV reared its head.
"You need something that has been around for generation upon generation," explains Christopher Duncan of the University of Liverpool, UK, who led the latest analysis. Plague fits the bill, he and his colleagues conclude from a mathematical modelling study published in the Journal of Medical Genetics1.
"You need something that has been around for generation upon generation."
Christopher Duncan, University of Liverpool, UK
Repeated outbreaks
Duncan's team points out that when the Black Death first struck, killing some 40% of Europeans between 1347 and 1350, only 1 person in 20,000 had the CCR5-32 mutation. As the centuries wore on, repeated outbreaks, culminating in the Great Plague of London in the 1660s, have occurred in tandem with rises in the mutation's frequency.
Other experts are not convinced, however. A similar study2 published in 2003 suggests that it was smallpox that boosted the mutation's frequency. "Smallpox would still be my favoured hypothesis," comments Neil Ferguson, an infectious disease expert at Imperial College in London, who was not involved in the study.
Duncan counters that smallpox has only been a serious threat in Europe since the 1600s, which may not have been enough time to have such a big genetic effect. But Ferguson argues that the influence of smallpox over the centuries may have been underestimated, because it largely affected children.
"Smallpox would still be my favoured hypothesis."
Neil Ferguson, Imperial CollegecLondon
"Smallpox seems the most parsimonious explanation," he adds. He points out that one major problem with Duncan's plague theory is that it requires a rethink of how plague was caused. If those with a virus-blocking mutation were more likely to survive, it follows that plague would have been caused by a virus. But the conventional view is that the plague epidemics of the Middle Ages were caused by a bacterium, Yersinia pestis.
Rats off the hook
Duncan admits that his theory is difficult to prove. But he argues that the outbreaks are easier to explain if one assumes that plague was passed directly from person to person as a virus, rather than the 'bubonic plague' that was caused by bacteria carried by rats and their fleas. "Rats are absolutely in the clear for Europe," he argues.
If that's true, then Duncan can explain not only the mutation's average levels in Europe, but also the fact that people in Finland and Russia have the highest level, around 16%, whereas a mere 4% of Sardinians possess it.
He points out that outbreaks of feverish viral disease continued in Scandinavia and Russia for far longer than in the rest of the continent, reinforcing the mutation's status as a valuable asset. "It was mouldering on until about 1800 in northern Europe."
References
1. Duncan S. R., Scott S. & Duncan C. J. J. Med. Genet. 42, 205 - 208 (2005).
2. Galvani A. P. & Slatkin M. Proc. Natl Acad. Sci. USA 100, 15276 - 15279 (2005).
中世紀(jì)瘟疫提高了歐洲人“抗艾”能力
據(jù)路透社報(bào)道，2005年第三期英國《醫(yī)學(xué)遺傳雜志》公布的一項(xiàng)研究結(jié)果稱,，中世紀(jì)時(shí)代歐洲大陸長期暴發(fā)的出血熱流行病為如今的歐洲居民提供了生物“選擇壓力”,，這使得當(dāng)今10%的歐洲居民對(duì)艾滋病病毒具有非常強(qiáng)的抵抗力。
在被命名為CCR5的細(xì)胞感受器中,，一種被稱為“Delta-32”的突變基因可保護(hù)人體免受艾滋病病毒感染,，和其他大陸居民相比，這種突變基因在歐洲居民人身上更為常見,。
科學(xué)家們以前認(rèn)為,，這種基因突變現(xiàn)象十分普遍，因?yàn)樗梢员Ｗo(hù)人們不受黑死病或天花流行病的侵襲,，而正常CCR5細(xì)胞感受器中的基因突變被認(rèn)為不具有這項(xiàng)功能,。
英國利物浦大學(xué)的科研人員通過電腦模擬公元1000到1800間歐洲人口統(tǒng)計(jì)數(shù)據(jù)發(fā)現(xiàn)，出血熱流行病的盛行,，加速了這種基因突變現(xiàn)象出現(xiàn)的頻率,，從過去黑死病流行時(shí)期的2萬分之一增加到了當(dāng)前的10分之一。
研究人員指出,，早從公元前1500年起,，致命性的病毒性出血熱就已經(jīng)開始在尼羅河谷出現(xiàn)了；公元前700-450年期間,，這種疫情又在美索不達(dá)米亞平原流行起來,；公元前430年，雅典也出現(xiàn)了出血熱,；公元541-700年間,，東羅馬帝國也暴發(fā)了出血熱疫情；公元627-744年間,，早期的伊斯蘭帝國流行起出血熱疫情,。英國科研人員解釋說,，1347到1665年間，歐洲大陸持續(xù)發(fā)生出血熱疫情,，CCR5細(xì)胞感受器成為出血熱病毒侵入人體的入口,。
科研人員指出，盡管1665年倫敦大瘟疫高峰早已經(jīng)成為歷史,，但出血熱這種疫情并非徹底消失了,。
利物浦大學(xué)生物學(xué)院教授克里斯托弗·鄧肯最后表示：“1665-1666年倫敦出血熱大瘟疫并沒有完全消失，后來繼續(xù)在瑞典,、丹麥,、俄羅斯、波蘭和匈牙利等國流行,，這種情況一直持續(xù)到1800年,。
出血熱瘟疫的繼續(xù)存在，為人類基因突變提供了連續(xù)不斷的選擇壓力,，這就是今天CCR5-Delta-32突變基因在斯堪的納維亞和俄羅斯出現(xiàn)頻率最高的原因,。”
