经济学人官方译文 | 流感如何进化:流感的成功很大程度上归功于它的易变性

How influenza evolves
流感如何进化
Mind your H’s and N’s
注意你的H和N
Flu’s success owes much to its genetic mutability
流感的成功很大程度上归功于它的易变性

BOTH “mini-epidemics” of seasonal flu, which happen most years, and much larger pandemics, of which 1918’s was the worst example, are the result of an arms race between the influenza virus and the immune systems of the animals it infects. Here’s how it works.
无论是大多数年份里都会发生的“小范围流行”的季节性流感,还是规模大得多的流感大流行(最严重的一次发生在1918年),都是流感病毒与它所感染的动物的免疫系统之间军备竞赛的结果。我们来看看流感病毒的作用机制。

Type A flu viruses—those which cause pandemics, and also most seasonal flu, have two important surface proteins, haemagglutinin (H) and neuraminidase (N). Haemagglutinin helps the virus invade a target cell. Neuraminidase helps new virus particles break out of that cell. These two proteins are also antigens, meaning that they are parts of a virus that may be recognised and reacted to by the immune system.
甲型流感病毒引起大范围流行和大部分季节性流感,它有两种重要的表面蛋白:血凝素(haemagglutinin,H)和神经氨酸酶(neuraminidase,N)。血凝素帮助病毒入侵目标细胞。神经氨酸酶帮助新的病毒颗粒从细胞中分离出来。这两种蛋白质也是抗原,也就是说,免疫系统或许可以识别出病毒中的这两种物质并做出反应。

But the process by which a flu virus hijacks a host cell’s molecular machinery in order to reproduce itself cuts out of the loop what are known as proofreading enzymes. The virus’s genetic material is thus copied with low fidelity, meaning proteins derived from it vary considerably in detail. That variability generates antigens which immune systems do not always recognise and react to immediately. Each year’s seasonal virus is therefore slightly different, and thus requires an updated vaccine—which is not true for most antiviral vaccinations.
但是,流感病毒会劫持宿主细胞的分子机制以自我复制,这一过程切断了那些具有校正功能的酶的回路。因此,病毒的遗传物质复制的保真度很低,这使得复制产生的蛋白质在细节上差异很大。这种多变性令生成的抗原并不总能被免疫系统识别并立即做出反应。因此每年的季节性流感病毒都略有不同,所以需要更新疫苗,而大多数抗病毒疫苗接种不需要这么做。

Pandemic viruses represent bigger shifts in this process. These create antigens sufficiently novel that have been given numbers by virologists (eg, N1, H3). Many hosts’ defences are unprepared for such big shifts, which happen, on average, three or four times a century. The 1918 pandemic was caused by a strain with a version of haemagglutinin called H1 and a version of neuraminidase called N1. The two subsequent flu pandemics of the 20th century, in 1957 and 1968, were caused by viruses carrying H2 and H3 antigens respectively, in combination with N2.
引起大范围流行的病毒在这一过程中出现的变异更大。它们产生的抗原非常新颖,已经由病毒学家编号(如N1、H3)。许多宿主的免疫系统对这样的大转变毫无准备,而这种转变平均每一百年会发生三到四次。1918年的流感大流行是由携带H1型血凝素和N1型神经氨酸酶的病毒株引起。20世纪在此之后爆发的两场流感大流行(分别在1957年和1968年)则分别由H2和H3型抗原与N2型抗原组合形成的病毒株引起。

Much of this mutating goes on outside human beings. Influenza is primarily an infection of birds, especially waterfowl. In these animals the virus infects the digestive system rather than the respiratory tract, usually without producing signs of malaise. Occasionally a bird-flu strain arises with molecular tools that enable it to infect people—the H5N1 and H7N9 strains are currently worrying disease-surveillance experts.
这种变异大部分发生在人类之外。流感主要感染鸟类,尤其是水禽。在这类动物中,病毒感染消化系统而不是呼吸道,通常不会产生不适的迹象。偶尔会出现可以通过分子工具感染人类的禽流感毒株。目前让疾病监测专家感到担忧的这类毒株是H5N1和H7N9。

The virus sometimes jumps directly from a bird (often a chicken) to a person, but more usually passes via a pig. The cells lining bird guts and human lungs are built differently, meaning that the virus needs different sets of tools to invade them. Pig-lung cells, sharing properties of both, act as intermediaries in which the virus can adapt from one to the other. Even after it has infected a human being, though, a virus cannot go on to cause a pandemic unless it also acquires the ability to pass easily between people. Fortunately, this is something H5N1 and H7N9 have yet to do.
这些病毒有时会直接从鸟类(通常是鸡)传染给人,但更多时候是通过猪传播。构成鸟类消化道内壁的细胞和人类肺部内壁的细胞结构不同,病毒需要不同的工具来入侵它们。猪的肺细胞兼具鸟类细胞和人类细胞的特性,因而成为病毒从适应鸟消化道细胞到适应人类肺细胞的中间宿主。不过,即便在病毒感染了人类之后,它也无法继续引起大范围流行,除非它还能获得在人与人之间轻易传播的能力。幸运的是,H5N1和H7N9还没能做到。