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科學技術
Flu
流感
How to make bird flu fly, part one
怎樣讓禽流感在人間傳播：步驟一
The first of two controversial research papers is published
兩個關于禽流感研究的論文一直備受爭議，現在其中之一已經公開發表了
ON APRIL 27th, after much toing and froing, the Dutch government gave Ron Fouchier of the Erasmus Medical Centre in Rotterdam permission to submit his paper on bird flu to Science.
今年4月27日，經過長久的等待之后，荷蘭政府批準了羅恩·富希恩在《科學》雜志上發表他關于禽流感研究的論文。羅恩·富希恩效力于鹿特丹的伊拉茲馬斯醫學院中心。
Dr Fouchier is the head of one of two groups studying how bird flu might become transmissible between people.
富希恩博士是兩個研究禽流感如何變得可以在人間傳播的團隊的領導者。
In December the authorities in America and the Netherlands prevented both his group and the other, led by Yoshihiro Kawaoka of the University of Wisconsin-Madison, from publishing their findings, lest they get into the wrong hands.
去年12月，美國和荷蘭有主管部門，由于擔心被誤用，而不允許了他的團隊和另一個由威斯康星大學麥迪遜分校的河岡義裕領導的團隊發表他們的研究成果。
This official fear stemmed from the deadly nature of bird flu.
官方的恐懼來自于自然界禽流感的致死性。
Of the 602 human cases reported since 2003, 355 have been fatal.
從2003年起，已有602例人感染禽流感的安全，其中355人已經死亡。
The factor that has stopped the death toll being worse is that people have to catch the virus directly from a bird.
為了阻止死亡人數增長，人們一不得不直接從鳥類身上提取病毒，這一點使得恐懼加深了。
It rarely, if ever, passes from one person to another.
盡管禽流感在人間傳播的情況十分罕見，但并非沒有。
Science has yet to publish Dr Fouchier's manuscript, but its rival Nature has gone ahead and published Dr Kawaoka's.
《科學》雜志已經公開了富希恩博士的手稿，但這之前它的老對手《自然》雜志已經搶先公開了河岡博士的論文。
This paper got clearance from the American authorities on April 20th.
美國的主管部門于4月20日發出了放行令。
So it is now possible to see what all the fuss was about.
因此我們現在可以了解其中的爭論是些什么。
Dr Kawaoka was interested in the role a protein called haemagglutinin plays in the transmission of avian influenza.
河岡博士關注一種稱為血凝素的蛋白質在禽流感傳播中的作用。
HA is the viral equivalent of a grappling hook:
HA處于病毒一方，像一個錨一樣：
it lets the virus latch onto a cell by binding to substances called sialic acids that are found in receptors on the cell's surface.
它通過綁定受體細胞表面的唾液酸，使得病毒抓緊細胞。
This done, the virus infects the cell with its DNA.
這樣做，接下來病毒就可以以其DNA感染細胞了。
But because the sialic acid found in birds is chemically different from that in mammals,
但是由于禽類身上發現有唾液酸在化學成份上不同于哺乳類的，
and because bird flu has evolved to recognise only the avian variety, it cannot stick easily to mammalian cells,
也由于禽流感進化得只能識別禽類變種，所以HA吸附到哺乳類動物細胞上不那么容易，
limiting its ability to infect people.
也就是說它感染人類的能力十分有限。
The researchers wanted to know what it would take to enhance that ability.
研究人員想要了解HA怎樣才能提高這種能力。
They took the HA gene from avian influenza viruses found in Vietnam and made millions of mutant versions, each of which was spliced back into a copy of the original virus.
他們將在越南發現的禽流感病毒中的HA基因提取出來，并制造了數百萬個變種，又把每一個插回到原來的病毒當中。
They then screened 2.1m of these mutant viruses to see which bind to sialic acid of the mammalian variety.
之后，他們掃描了二百一十萬個變種病毒，看看它們中的哪一個可以與哺乳動物的唾液酸綁定。
Just eight can do so, and just one of those has become, in effect, a mammalian specialist, because it can no longer bind to avian cells.
其中只有8個能這樣，而且只有其中之一實際上變得不再能綁定禽類細胞，而變成了專門綁定哺乳動物品種。
Dr Kawaoka decided to concentrate his efforts on this specialist. Further tests revealed that two mutations in its HA gene, called N224K and Q226L, were responsible for its characteristics.
河岡博士決定集中精力研究這個特別的品種。進一步的測試顯示，其中有兩種HA基團的變種，N224K和Q226L，是它們決定了HA的特性。
It is here that things get complicated.
此時情況變得復雜起來。
Instead of looking at the doubly mutated gene in bird flu, the team transplanted it into the virus that caused the human-flu pandemic of 2009.
這個團隊將這種基因引入2009年引起人禽流感傳播的病毒中，而不僅僅是去評判那些成倍變異的禽流感基因。
By doing so, they virtually guaranteed they would make a virus that could pass between mammals.
這樣，使得他們實際上能夠制造出測定哺乳動物間傳播的禽流感病毒。
And so it proved.
最終，這也得到了證實。
When they tested it on ferrets, it passed through the air from one animal to another.
當他們在雪貂身上進行測試后，病毒經過空氣從一只傳到另一只。
Moreover, closer inspection showed that two other mutations, N158D and T318I, had spontaneously got tangled up in the mix.
此外，進一步檢測顯示，另外兩種變種，即N158D和T318I，同時也緊緊糾纏于病毒中。
What all this means, then, is slightly obscure.
實驗的結果看起來有點晦澀。
Dr Kawaoka's purpose was to study how the mammalian-transmission mutations worked.
河岡博士的目的是研究哺乳動物間傳播的變種如何起作用。
In this, he succeeded.
在這一點上他成功了。
He found that N224K, Q226L and N158D all control areas in the head of the HA protein—ie, the hook—and probably help it attach to the mammalian flavour of sialic acid.
他發現了N224K、Q226L和N158D位于HA蛋白頭部的控制區，它們有可能幫助HA偏好于哺乳動物的唾液酸。
T318I controls part of HA's stem and may help to stabilise the protein as it injects viral DNA into cells.
T318I控制HA的根部，使得HA能在病毒向細胞中注入DNA時保持穩定。
By transferring the genes into a virus that was known to be good at moving between mammals,
通過將這些基因轉錄入病毒，使其易于在哺乳動物間傳播。
Dr Kawaoka has shown that the HA gene is not itself an obstacle to bird flu gaining that ability, though its other genes may be.
這樣，河岡博士證實了HA基因本身并不是禽流感病毒獲得這種能力的障礙，盡管其他基因或許是。
Perhaps Dr Fouchier's paper will shed more light on the matter.
或許富希恩博士的論文將會為此提供線索。
