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Science and technology.
科技。
Flu research.
流感研究。
How to make bird flu fly, part one.
让禽流感飞起来，第一部分。
The first of two controversial research papers is published.
充满争议的两篇研究论文的其中之一已发表。
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. Dr Fouchier is the head of one of two groups studying how bird flu might become transmissible between people. 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. This official fear stemmed from the deadly nature of bird flu. Of the 602 human cases reported since 2003, 355 have been fatal. The factor that has stopped the death toll being worse is that people have to catch the virus directly from a bird (usually a chicken). It rarely, if ever, passes from one person to another.
经过了几番周折，荷兰政府终于在4月27日允许鹿特丹伊拉斯谟医学中心的罗恩?富希耶将其关于禽流感研究的文章投稿给《科学》杂志。现今有两个科研团队正致力于研究禽流感在人群中传播的可能性，富希耶是其中一个团队的领导者。在去年12月，美国和荷兰当局阻止富希耶团队和由威斯康星大学的河冈义裕所带领的另一团队发表有关的研究发现，以免这些信息流入不法之徒手中。官方的这种恐怖来源于禽流感的高致死性。自2003年来报告的602个禽流感病例中，死亡病例达355个。死亡数目之所以不再进一步恶化，是因为人只有与鸟类（通常是鸡）直接接触才会感染病毒。该病毒很少且几乎不会在人群中直接传播。
Science has yet to publish Dr Fouchier's manuscript, but its rival Nature has gone ahead and published Dr Kawaoka's. This paper got clearance from the American authorities on April 20th. So it is now possible to see what all the fuss was about.
《科学》杂志还没有发表富希耶的文章，但其对手《自然》杂志已抢先一步发表了河冈义裕的文章。美国当局于4月20日批准了该文章的发表。因而现在我们就能知道人们为何大惊小怪了。
Dr Kawaoka was interested in the role a protein called haemagglutinin (HA) plays in the transmission of avian influenza. HA is the viral equivalent of a grappling hook: 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. This done, the virus infects the cell with its DNA. But because the sialic acid found in birds is chemically different from that in mammals, and because bird flu has evolved to recognise only the avian variety, it cannot stick easily to mammalian cells, limiting its ability to infect people.
河冈义裕对一种叫做血凝素（HA）的蛋白质在禽流感传播中所起的作用而感兴趣。血凝素是病毒中一种类似于爪钩的物质：它通过抓住一种位于细胞表面受体中称作唾液酸的物质而使病毒与细胞相黏附。一旦黏附过程完成，病毒就开始以其自身DNA感染细胞。但由于鸟类细胞中唾液酸的化学成分不同于哺乳动物，且演化的禽流感病毒只能识别鸟类细胞，因而禽流感病毒无法轻易地粘附于哺乳动物细胞上，使得其感染人类的能力大大受限。
The researchers wanted to know what it would take to enhance that ability. 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. They then screened 2.1m of these mutant viruses to see which bind to sialic acid of the mammalian variety. 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.
研究者们希望知道如何能增强禽流感病毒的感染人类能力。他们提取出于越南发现的禽流感病毒中的血凝素基因，然后将其改造生成了数百万种突变类型，接着将每一种突变类型与复制的原始病毒相接合。他们筛选了210万种突变病毒以找到能与哺乳动物细胞的唾液酸相接的病毒。最终只有8种突变病毒可以做到，且事实上只有一种突变病毒变成了感染哺乳动物的专家，因为其不再黏附于鸟类细胞。
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.
河冈义裕决定致力于此种病毒的研究。进一步的试验揭示出，其血凝素基因中分别称为N224K 和Q226L的两个变异基因是引起此病毒特性的主要因素。
It is here that things get complicated. 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. By doing so, they virtually guaranteed they would make a virus that could pass between mammals.
然而事情就是在此时变得复杂起来。这支团队并没有继续研究这种禽流感病毒中的双重变异基因，而是将其移植到引起2009年猪流感流行的病毒中。他们这种做事实上是证明了他们能制造出一种在可在哺乳动物间传播的病毒。
And so it proved. When they tested it on ferrets (often used as proxies for people in these sorts of studies), it passed through the air from one animal to another. Moreover, closer inspection showed that two other mutations, N158D and T318I, had spontaneously got tangled up in the mix.
而他们确实也做到了。通过在雪貂（在此类实验中通常用来代替人类）身上的实验证明，此病毒能通过空气在动物之间传播。此外，进一步观察表明，两种其他的变异基因—N158D和T318I也自发地产生并整合入已变异的病毒基因中。
What all this means, then, is slightly obscure. Dr Kawaoka's purpose was to study how the mammalian-transmission mutations worked. In this, he succeeded. 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. T318I controls part of HA's stem and may help to stabilise the protein as it injects viral DNA into cells.
那么这一切的意义让人有些费解。河冈义裕的意图是研究这些变异的基因如何能在哺乳动物间传播。在这方面，他成功了。他发现N224K, Q226L和N158D这三种基因都能控制血凝素蛋白的头部—即爪部—且可能可以帮助血凝素与哺乳动物的唾液酸相连。T318I则控制血凝素的茎部，当病毒往细胞中注入病毒DNA时能稳定血凝素。
By transferring the genes into a virus that was known to be good at moving between mammals, 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. Perhaps Dr Fouchier's paper will shed more light on the matter.
通过将这些基因转移到易于在哺乳动物间传播的病毒中，河冈义裕证明了血凝素基因本身并不是阻止禽流感在人群中传播的障碍，而其他基因可能才是。可能富希耶的文章能在这个问题上给我们更多的启示。
