经济学人下载:怎样让禽流感在人间传播

Science and technology
科学技术

Flu
流感

How to make bird flu fly, part one
怎样让禽流感在人间传播：步骤一

The first of two controversial research papers is published
两个关于禽流感研究的论文一直备受争议，现在其中之一已经公开发表了

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，经过长久的等待之后，荷兰政府批准了罗恩·富希恩在《科学》杂志上发表他关于禽流感研究的论文。罗恩·富希恩效力于鹿特丹的伊拉兹马斯医学院中心。

Dr Fouchier is the head of one of two groups studying how bird flu might become transmissible between people.
富希恩博士是两个研究禽流感如何变得可以在人间传播的团队的领导者。

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，美国和荷兰有主管部门，由于担心被误用，而不允许了他的团队和另一个由威斯康星大学麦迪逊分校的河冈义裕领导的团队发表他们的研究成果。

This official fear stemmed from the deadly nature of bird flu.
官方的恐惧来自于自然界禽流感的致死性。

Of the 602 human cases reported since 2003, 355 have been fatal.
从2003年起，已有602例人感染禽流感的安全，其中355人已经死亡。

The factor that has stopped the death toll being worse is that people have to catch the virus directly from a bird.
为了阻止死亡人数增长，人们一不得不直接从鸟类身上提取病毒，这一点使得恐惧加深了。

It rarely, if ever, passes from one person to another.
尽管禽流感在人间传播的情况十分罕见，但并非没有。

Science has yet to publish Dr Fouchier's manuscript, but its rival Nature has gone ahead and published Dr Kawaoka's.
《科学》杂志已经公开了富希恩博士的手稿，但这之前它的老对手《自然》杂志已经抢先公开了河冈博士的论文。

This paper got clearance from the American authorities on April 20th.
美国的主管部门于4月20日发出了放行令。

So it is now possible to see what all the fuss was about.
因此我们现在可以了解其中的争论是些什么。

Dr Kawaoka was interested in the role a protein called haemagglutinin plays in the transmission of avian influenza.
河冈博士关注一种称为血凝素的蛋白质在禽流感传播中的作用。

HA is the viral equivalent of a grappling hook:
HA处于病毒一方，像一个锚一样：

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.
它通过绑定受体细胞表面的唾液酸，使得病毒抓紧细胞。

This done, the virus infects the cell with its DNA.
这样做，接下来病毒就可以以其DNA感染细胞了。

But because the sialic acid found in birds is chemically different from that in mammals,
但是由于禽类身上发现有唾液酸在化学成份上不同于哺乳类的，

and because bird flu has evolved to recognise only the avian variety, it cannot stick easily to mammalian cells,
也由于禽流感进化得只能识别禽类变种，所以HA吸附到哺乳类动物细胞上不那么容易，

limiting its ability to infect people.
也就是说它感染人类的能力十分有限。

The researchers wanted to know what it would take to enhance that ability.
研究人员想要了解HA怎样才能提高这种能力。

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.
他们将在越南发现的禽流感病毒中的HA基因提取出来，并制造了数百万个变种，又把每一个插回到原来的病毒当中。

They then screened 2.1m of these mutant viruses to see which bind to sialic acid of the mammalian variety.
之后，他们扫描了二百一十万个变种病毒，看看它们中的哪一个可以与哺乳动物的唾液酸绑定。

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个能这样，而且只有其中之一实际上变得不再能绑定禽类细胞，而变成了专门绑定哺乳动物品种。

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.
河冈博士决定集中精力研究这个特别的品种。进一步的测试显示，其中有两种HA基团的变种，N224K和Q226L，是它们决定了HA的特性。

It is here that things get complicated.
此时情况变得复杂起来。

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.
这个团队将这种基因引入2009年引起人禽流感传播的病毒中，而不仅仅是去评判那些成倍变异的禽流感基因。

By doing so, they virtually guaranteed they would make a virus that could pass between mammals.
这样，使得他们实际上能够制造出测定哺乳动物间传播的禽流感病毒。

And so it proved.
最终，这也得到了证实。

When they tested it on ferrets, it passed through the air from one animal to another.
当他们在雪貂身上进行测试后，病毒经过空气从一只传到另一只。

Moreover, closer inspection showed that two other mutations, N158D and T318I, had spontaneously got tangled up in the mix.
此外，进一步检测显示，另外两种变种，即N158D和T318I，同时也紧紧纠缠于病毒中。

What all this means, then, is slightly obscure.
实验的结果看起来有点晦涩。

Dr Kawaoka's purpose was to study how the mammalian-transmission mutations worked.
河冈博士的目的是研究哺乳动物间传播的变种如何起作用。

In this, he succeeded.
在这一点上他成功了。

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.
他发现了N224K、Q226L和N158D位于HA蛋白头部的控制区，它们有可能帮助HA偏好于哺乳动物的唾液酸。

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能在病毒向细胞中注入DNA时保持稳定。

By transferring the genes into a virus that was known to be good at moving between mammals,
通过将这些基因转录入病毒，使其易于在哺乳动物间传播。

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.
这样，河冈博士证实了HA基因本身并不是禽流感病毒获得这种能力的障碍，尽管其他基因或许是。

Perhaps Dr Fouchier's paper will shed more light on the matter.
或许富希恩博士的论文将会为此提供线索。