中国科学院大学研究生学术英语读写教程 Unit6 Biology TextA 原文和翻译
中国科学院大学研究生学术英语读写教程
Unit6 Biology TextA 原文和翻译
Coincidental Killers
巧合杀手
Ed Young
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In the late 17th century, the Dutch scientist Antonie van Leeuwenhoek created a new type of microscope lens and brought an entire world of tiny organisms into focus. Looking at his own dental plaque, he wrote: “I then most always saw with great wonder, that in the said matter there were many very little living animalcules, very prettily a-moving.” These little creatures were intriguing but seemingly unimportant, and few others picked up the baton from van Leeuwenhoek. That changed in the 19th century, when Louis Pasteur and Robert Koch proved that some of these microbes were behind important diseases.
17 世纪末，荷兰科学家安东尼·范·列文虎克发明了一种新型显微镜镜头，将整个微生物世界都聚焦在了眼前。他看着自己的牙菌斑，写道：“我当时总是惊奇地发现，牙菌斑里有许多非常小的活微生物，它们活动得非常漂亮。”这些小生物很有趣，但似乎并不重要，很少有人能从范·列文虎克手中接过接力棒。这种情况在 19 世纪发生了改变，路易斯·巴斯德和罗伯特·科赫证明其中一些微生物是导致重大疾病的元凶。
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That framing has stuck. Microbes are everywhere, but we take their presence on phones, keyboards, and toilet seats as a sign of filth and squalor. They fill our bodies, helping us to digest our food and safeguard our health, but we view them as adversaries to be drugged and conquered.
这种观念根深蒂固。微生物无处不在，但我们却把它们出现在手机、键盘和马桶座上，视为肮脏和肮脏的标志。它们充斥着我们的身体，帮助我们消化食物，保障我们的健康，但我们却把它们视为需要用药物征服的敌人。
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This antagonism is understandable. Aside from those of us with access to microscopes, most people will never see microbes with their own eyes. And so we tend to identify microbes with the disease-causing minority among them, the little buggers that trigger the tickling mist of a sneeze or the pustule on otherwise smooth skin. We become aware of their existence when they threaten our lives, and for much of our history, that threat was substantial. Epidemics of smallpox, cholera, tuberculosis, and plague have traumatised humanity, and the fear of these diseases has contaminated our entire culture, from our religious rites to Hollywood films such as 8 Contagion (2012) or Outbreak (1995).
这种敌意是可以理解的。除了那些能用显微镜观察的人，大多数人永远不会亲眼看到微生物。因此，我们倾向于将微生物与其中的致病少数群体联系起来，这些小虫子会引发打喷嚏时产生的痒痒的雾气，或者在原本光滑的皮肤上长出脓疱。当它们威胁到我们的生命时，我们就会意识到它们的存在，而在我们的大部分历史中，这种威胁是巨大的。天花、霍乱、肺结核和瘟疫的流行给人类带来了创伤，对这些疾病的恐惧已经污染了我们的整个文化，从我们的宗教仪式到好莱坞电影，如《传染病》（2012 年）或《极度恐慌》（1995 年）。
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When microbes aren’t killing us, we are largely oblivious to them. So, we construct narratives of hosts and pathogens, heroes and villains, us and them. Those that cause disease exist to reproduce at our expense, and we need new ways of resisting them. And so we study how they evolve to outfox our immune system or to spread more easily from one person to another. We identify genes that allow them to cause disease and we label those genes as “virulence factors”. We place ourselves at the centre of their world. We make it all about us.
当微生物没有杀死我们时，我们基本上对它们视而不见。因此，我们构建了宿主和病原体、英雄和恶棍、我们和它们的故事。那些导致疾病的微生物以牺牲我们为代价而繁殖，我们需要新的方法来抵抗它们。因此，我们研究它们如何进化以超越我们的免疫系统或更容易在人与人之间传播。我们识别出使它们致病的基因，并将这些基因标记为“毒力因子”。我们将自己置于它们世界的中心。我们让它们成为我们自己的一切。
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But a growing number of studies show that our anthropocentric view is sometimes unjustified. The adaptations that allow bacteria, fungi and other pathogens to cause us harm can easily evolve outside the context of human disease. They are part of a microbial narrative that affects us, and can even kill us, but that isn’t about us. This concept is known as the coincidental evolution hypothesis or, as the Emory University microbiologist Bruce Levin described it in 2008, the “shit happens” hypothesis.
但越来越多的研究表明，我们的人类中心主义观点有时是不合理的。允许细菌、真菌和其他病原体对我们造成伤害的适应性很容易在人类疾病的背景之外进化。它们是影响我们甚至可能杀死我们的微生物叙事的一部分，但这与我们无关。这一概念被称为巧合进化假说，或者如埃默里大学微生物学家布鲁斯·莱文在 2008 年所描述的那样，“糟糕的事情发生了”假说。
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This hypothesis does not apply to all infections, and is almost certainly irrelevant to viruses, which always need to reproduce in a host. Nor does it apply to the many bacteria and fungi, such as Staphylococcus aureus or Candida albicans, that are long-standing human pathogens and well-adapted to us. But it does explain some weird aspects of many diseases.
这一假设并不适用于所有感染，而且几乎肯定与病毒无关，因为病毒总是需要在宿主体内繁殖。它也不适用于许多细菌和真菌，如金黄色葡萄球菌或白色念珠菌，它们是长期存在的人类病原体，并且对我们适应得很好。但它确实解释了许多疾病的一些奇怪之处。
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Why, for example, would bacteria harm the hosts that they depend on for survival? In some cascs, the answer is obvious: They cause symptoms such as sneezing or coughing that help them to spread. But what about S.pneumoniae? Strains that sit harmlessly in a host’s airways are already capable of spreading to another individual. The virulent forms, which descend deeper into the respiratory tract, are actually less contagious. The same goes for bugs such as Hemophilus influenzae and Neisseria meningitidis, which can inflame the protective membranes around the brain and lead to life-threatening cases of bacterial meningitis. In doing so, they risk capsizing their own ship without any hope of boarding a new one.
例如，为什么细菌会伤害它们赖以生存的宿主？在某些情况下，答案是显而易见的：它们会引起打喷嚏或咳嗽等症状，从而帮助它们传播。但是肺炎链球菌呢？在宿主呼吸道中无害的菌株已经能够传播给另一个人。而深入呼吸道的毒性菌株实际上传染性较弱。流感嗜血杆菌和脑膜炎奈瑟菌等细菌也是如此，它们会使大脑周围的保护膜发炎，导致危及生命的细菌性脑膜炎。这样做，它们就有倾覆自己的船的风险，而没有希望登上另一艘船。
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The coincidental evolution hypothesis helps to resolve these paradoxes. It tells us that at least some human diseases have nothing to do with us at all.
巧合进化假说有助于解决这些悖论。它告诉我们，至少有些人类疾病与我们根本无关。
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The coincidental evolution hypothesis explains a number of other recent discoveries about microbes. Scientists have found antibiotic resistance genes in bacteria that have been frozen for 30,000 years, or isolated in million-year-old caves. We might think of antibiotics as modern inventions, but they’re actually weapons that bacteria have been using against each other for aeons, or at least well before Alexander Fleming noticed a funky mould in a Petri dish in 1928. Antibiotic resistance genes evolved as part of this ancient war, but they also help today’s microbes to deal with the medicines that we mass-produce.
巧合进化假说解释了最近关于微生物的许多其他发现。科学家在冷冻了 3 万年或分离在百万年前的洞穴中的细菌中发现了抗生素抗性基因。我们可能认为抗生素是现代发明，但它们实际上是细菌之间长久以来一直在使用的武器，至少在 1928 年亚历山大·弗莱明在培养皿中发现奇怪的霉菌之前就已经存在了。抗生素抗性基因是这场古老战争的一部分，但它们也帮助当今的微生物对付我们大量生产的药物。
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Likewise, many of the “virulence genes” that help pathogens to cause disease have counterparts in marine microbes with no track record of infecting humans. And some supposedly pathogenic bacteria were often common parts of the environment. “These organisms become accidental pathogens,” says the microbiologist Arturo Casadevall from Yeshiva University in New York. “They’ll still be there even if you remove all the animals from the planet. And yet, evolution selected for just the right combination of traits to cause disease in humans.”
同样，许多帮助病原体致病的“毒力基因”在海洋微生物中也有对应基因，而这些微生物并没有感染人类的记录。一些所谓的致病细菌往往是环境中的常见部分。“这些生物会成为意外的病原体，”纽约叶史瓦大学的微生物学家阿图罗·卡萨德瓦尔说。“即使你从地球上消灭了所有的动物，它们仍然会存在。然而，进化选择了恰好合适的特征组合来导致人类患病。”
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Vibrio cholerae, the bacterium that causes cholera, is a good example. Scientists used to regard it as a human pathogen that spreads when the faeces of infected people seep into water supplies. We now know that it’s mainly a marine species that attaches itself to the shells of small crustaceans, and occasionally makes its way into our water supply. “In the last decade, people have begun to accept that a lot of these opportunistic pathogens that people assumed were only in the environment transiently between human hosts are actually environmental bacteria that occasionally end up in humans,” says Diane McDougald from the University of New South Wales, who studies V.cholerae.
引起霍乱的霍乱弧菌就是一个很好的例子。科学家过去认为它是一种人类病原体，当感染者的粪便渗入水源时就会传播。我们现在知道它主要是一种海洋生物，附着在小型甲壳类动物的壳上，偶尔会进入我们的水源。“在过去十年里，人们开始接受这样一个事实：许多人们认为只会在人类宿主之间短暂存在的机会性病原体实际上是偶尔进入人类的环境细菌，”新南威尔士大学研究霍乱弧菌的黛安·麦克杜格尔德说。
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Many of the pathogens we fear most are mere tourists on the human body. Their real homes are oceans, caves, or soils. To understand them, we need to understand them within their natural ecology. Soil, for example, is an extreme habitat for a microbe: harsh and constantly changing. It can quickly oscillate from flood to drought, from scalding heat to freezing cold, and total darkness to intense solar radiation. It’s rife with other competing microbes, and crawling with hungry predators. We fear lions and tigers and bears; bacteria have to contend with phage viruses, nematode worms, and predatory amoebas.
我们最害怕的许多病原体只是人类身体上的过客。它们真正的家园是海洋、洞穴或土壤。要了解它们，我们需要了解它们的自然生态。例如，土壤是微生物的极端栖息地：严酷且不断变化。它可以从洪水到干旱、从灼热到严寒、从完全黑暗到强烈的太阳辐射迅速变化。它充满了其他竞争微生物，到处都是饥饿的捕食者。我们害怕狮子、老虎和熊；细菌必须与噬菌体病毒、线虫和捕食性变形虫抗衡。
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All of these conditions can lead to adaptations that make microbes accidentally suited for life in a human host. We are, after all, just another environment. A thick capsule that shields a microbe from dehydration could also shield it from our immune system. A spore that is adapted for travelling through the air can be easily inhaled into a respiratory tract.
所有这些条件都可能导致微生物发生适应，意外地适应在人类宿主体内生存。毕竟，我们只是另一个环境。保护微生物免于脱水的厚荚膜也可以保护它免受我们的免疫系统攻击。适合在空气中传播的孢子很容易被吸入呼吸道。
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Scientists have demonstrated many of these coincidental adaptations by exposing bacteria to a natural threat and showing that they then become better at infecting humans and other mammals. Escherichia coli, for example, is a common gut bacterium, and a darling of laboratory scientists. In its natural environments, whether the soil or the gut of a mammal, it is menaced by predatory amoebas, which threaten to engulf and digest it. In 2010, the French scientist Frantz Depaulis and colleagues found an E.coli strain called 536 that resists these predators, with genes that protect it from the amoebas’ digestive enzymes and allow it to scavenge nutrients such as iron. Rather than being disintegrated, it actually grows inside its would-be predator and eventually kills it from within.
科学家们已经证实了许多这样的巧合适应，他们将细菌暴露在自然威胁下，并表明它们随后更善于感染人类和其他哺乳动物。例如，大肠杆菌是一种常见的肠道细菌，也是实验室科学家的宠儿。在自然环境中，无论是土壤还是哺乳动物的肠道，它都受到掠食性变形虫的威胁，这些变形虫威胁着要吞噬和消化它。2010 年，法国科学家 Frantz Depaulis 和同事发现了一种名为 536 的大肠杆菌菌株，它可以抵抗这些捕食者的攻击，这种菌株的基因可以保护它免受变形虫消化酶的侵害，并允许它吸收铁等营养物质。它并没有被分解，而是在潜在捕食者体内生长，最终从内部杀死它。
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Many of these protective genes also allow strains of the mostly harmless E.coli to cause severe illness in humans, mice and other mammals. This makes perfect sense. Many of our immune cells, like macrophages, engulf and digest microbes just as amoebas do, so an amoeba-proof bacterium is also a macrophage-proof one. By adapting to their natural predators, strains of E.coli are coincidentally pre-adapted to foil our immune system.
许多保护性基因也使大肠杆菌菌株（这些菌株大多无害）导致人类、小鼠和其他哺乳动物患上严重疾病。这完全说得通。我们的许多免疫细胞（如巨噬细胞）会像变形虫一样吞噬和消化微生物，因此抗变形虫的细菌也是抗巨噬细胞的细菌。通过适应其天敌，大肠杆菌菌株恰好预先适应了挫败我们的免疫系统。
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The coincidental evolution hypothesis might be irksome to some. What are the odds that an adaptation to one challenge would perfectly predispose an organism to another? The answer, it seems, is: pretty high. Evolution, however, is all about small probabilities manifesting through long timescales and large numbers - and microbes have both. They have been living on the planet for billions of years, and there are countless legions of them.
巧合进化假说可能会让一些人感到厌烦。适应一种挑战会完全导致生物体适应另一种挑战的可能性有多大？答案似乎是：相当高。然而，进化全是关于通过长时间尺度和大量数量体现出来的小概率——微生物兼具这两种特性。它们已经在地球上生活了数十亿年，数量不计其数。
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Casadevall likes to say that each microbe holds a different hand of cards adaptations that allow it to cope with its environment. Most of these combinations are meaningless to us. A bacterium might be able to resist being digested by other cells, but it might not be able to grow at 37 degrees Celsius. It might grow at the right temperature, but it might not be able to tolerate our slightly alkaline pH levels. But that doesn’t matter. There are so many microbes out there that some of them will end up with a hand that lets them muscle their way into our game. “If you take all the microbial species in the world and imagine that they have these traits randomly, you can find pathogenic microbes for practically anything,” says Casadevall.
Casadevall 喜欢说，每种微生物都拥有不同的适应能力，以适应其环境。大多数这些组合对我们来说毫无意义。一种细菌可能能够抵抗被其他细胞消化，但它可能无法在 37 摄氏度下生长。它可能在合适的温度下生长，但它可能无法忍受我们略带碱性的 pH 值。但这并不重要。外面有这么多微生物，其中一些最终会得到一手好牌，让它们强行进入我们的游戏。Casadevall 说：“如果你把世界上所有的微生物物种都拿出来，想象它们随机拥有这些特征，你几乎可以找到任何致病微生物。”