VOA常速英语2017--HIV或越“变”越弱（在线收听）

HIV, the virus that causes AIDS, frequently mutates. That has allowed the virus to bypass the immune system and infect about 80 million people over the last 35 years. However, researchers say the rapid evolution of HIV actually may be reducing its ability to cause AIDS.

人类免疫缺陷病毒(Human Immunodeficiency Virus)是引发艾滋病的病毒，这种病毒变异频繁。这种特点就让它可以无视免疫系统，并在过去的35年中感染了近8千万人。不过，研究人员表示，该病毒的快速演变实际上可能会降低其引发艾滋病的能力。

Oxford University Professor Phillip Goulder, the lead scientist in the study, said, “One of the quintessential features of HIV is its ability to mutate and evade the best things we can throw at it, whether its immune responses or antiretroviral drugs. That’s its real strength.”

哈佛大学的菲利普教授是牵头该项研究的科学家，他说，“HIV的一个核心特征是它的变异能力和躲避能力，它能躲避开任何东西，包括免疫应答或抗逆转录药物。这是它的强大之处。”

But HIV is not omnipotent.

但HIV病毒也不是万能的。

“Even HIV has some weaknesses. The fact is there are some parts of the virus that really don’t like to change. And one of these regions is the central core that encapsulates the two copies of the viral RNA and the various viral enzymes. That region of the virus can mutate. But if it mutates it usually damages the ability of the virus to multiply, replicate, efficiently.”

“即便HIV也有自己的弱点。其实，这种病毒的某些部分厌恶改变。其中一处就是含有2个病毒性核糖核酸(RNA)复制体和多种病毒酶的核心部分。病毒的这一部分可以进行变异。但这个地方变异了，通常会破坏HIV有效繁殖和复制的能力。”

RNA is a molecule necessary in the production of proteins that are essential for life.

核糖核酸(RNA)是合成生命必须蛋白质的必要分子。

Goulder said the most effective responses to HIV target the capsid protein. It encloses the virus’ nucleic acid, which allows the transfer of genetic information between different generations of the virus.

菲利普教授说，对HIV病毒最有效的应答是攻击其衣壳蛋白质。衣壳蛋白质上有HIV的核酸，核酸是HIV传递遗传信息的关键。

HIV’s many mutations take their tol.

太多的变异反而降低了HIV的毒性。

“The accumulation of these mutations over time effectively results in a diminution of the ability of the virus to infect cells efficiently and to cause disease. So that’s a good thing.”

“经年累月的变异不断积累，最终降低了HIV有效感染细胞和引发疾病的能力。所以这是一件好事。”

HIV, he said, becomes less virulent, losing some ability to cause AIDS through the collapse of the immune system. But could HIV ever reach the point where it mutates into something that does not cause disease?

HIV病毒，他说，它的病毒性愈发降低，逐渐失去了其通过破坏免疫系统来引发艾滋病的能力。但HIV是否能变异到不再引发疾病的程度呢？

“It is but speculative to say what’s going to happen in 10 years of tens of decades. If the trend that we’ve seen in the last 10 years in Botswana were to continue – and I see no reason why it shouldn’t – I think the number of people who can control the virus through their immune system would definitely go up – or be expected to go up – and eventually could be some tens of decades down the track – the majority of people.”

“可以预测未来十年甚至几十年内将会发生什么。如果过去10年中我们在博茨瓦纳(非洲中南部国家)的所见能延续——我确实认为没有理由无法继续——那么我认为能通过自身免疫系统来控制HIV病毒的人数一定会上涨——或很有希望上涨——也可能最终要用上百年的时间——大多数人能做到。”

The research was based on the HIV-1 strain that typically infects people in southern Africa. Goulder pointed out that another strain of the virus, HIV-2, which occurs in West Africa, causes AIDS in a smaller fraction of people it infects.

该研究是以在南非感染无数人的HIV-1型流行株为研究对象的。菲利普指出，而感染HIV-2型流行株继而引发艾滋病的西非人数量要比前者少。

“You know, it’s not impossible to see HIV becoming less of a cause of disease. And that’s what you see in the monkeys who are naturally infected with SIV, the relation of HIV, which is where we actually got HIV from. They suffer no disease at all.”

“大家都知道，要让HIV不再引发艾滋病也不是不可能的。这一点我们在自然感染猿猴免疫缺损病毒(SIV, Simian Immunodeficiency Virus)的猴类身上已经得到了证实，而人类就是从猴类身上感染了SIV的相关病毒HIV的。如今猴类已不再受SIV的侵扰了。”

SIV stands for Simian Immunodeficiency Virus.

SIV是Simian Immunodeficiency Virus的缩写。

Professor Goulder also said the greater use of antiretroviral drugs appears to affect the virulence of HIV. The drugs may accelerate the evolution of those HIV variations that have a “weaker ability to replicate.”

菲利普教授还说，加大抗逆转录药物的使用似乎影响了HIV的毒性。这种药物可能让HIV加速演化为变种，而变种“繁殖的能力更弱。”

The findings appear in the journal Proceedings of the National Academy of Sciences. Goulder and his Oxford colleagues worked with scientists from South Africa, Canada and Japan, as well as Harvard University and Microsoft Research.

上述发现已发表在《美国国家科学院院刊》上。这是菲利普教授及其哈佛同事与来自南非、加拿大、日本以及哈佛大学和微软研究院的科学家一道合作的结果。