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今读到最新一期出版的“经济学家”Economist 杂志刊登了一篇题目为“展望未来” 的文章,本人认为非常有看点,全文阐述了第19届国际艾滋病会议的宗旨,同时也探讨了治疗艾滋病的最新发展动向。本人试着将全文分段做了翻译,目的是想引起人们对艾滋病治疗的关注同时也想同广大爱好翻译的朋友们进行学习交流。如果您对本人的翻译内容有异议或有更好的翻译方法请直接提供上来,相信对我本人也是一次学习的机会。由于我个人水平有限,其中会有错译、漏译或理解上的错误出现,希望诸位高手谅解且多多指教!

Looking into the future 展望未来

Jul 28th 2012 | WASHINGTON, DC | from the print edition (原自经济学家杂志)

Now that the means exist to bring AIDS under control, attention is turning towards a cure


“CAN AIDS be cured?” That was the question being whispered in the back rooms and satellite meetings of the 19th International AIDS Conference, held in Washington, DC, this week. The conference’s formal business was to keep up the momentum behind the most successful public-health campaign of the past 30 years: the taming, at the cost of a few pills a day, of an infection that was once an inevitable killer. It still kills. About 1.7m people succumbed last year. But that figure is down from 2.3m in 2005 (see chart 1), and is expected to continue falling. Now, therefore, some people are starting to look beyond the antiretroviral (ARV) drugs which have brought this success. They are asking if something else could do even better.


The drugs work, and are getting cheaper by the year: a report released during the conference by the Clinton Foundation, an American global-health charity, put the annual cost of treatment at $200; it used to be $10,000. But once on them, you are on them for life. Stop, and the virus crawls out of cellular hidey-holes that ARVs cannot reach and rapidly reinfects you. This has implications both for patients, whose lives are constrained by the need for constant medication, and taxpayers, who bear most of the cost of this indefinite treatment.

推出各种治疗药物且价格逐年变得更便宜。与会期间一份由美国全球健康慈善机构-克林顿基金会提供的报告显示,过去治疗费用一年要花费1万美元,而如今一年才要200美元,不过问题是一旦开始用药就不能停,要终身服用。令人纠结的是艾滋病病毒是从细胞隐藏洞里爬出来的,而抗病毒逆转药类物无法进入,所以,当病毒一旦出现病患者会又一次被感染 。这就意味着病患者要想活命就必须不终断的进行治疗,而对于纳税者们来说要承担这些患者永久治疗的大部分费用。

Many of those taxpayers do not live in the rich world but in the worst-afflicted countries. A new estimate by UNAIDS, the United Nations agency charged with combating the disease, suggests that more than half of the cost of treating and preventing AIDS is now borne by these countries, rather than paid for by international agencies (see chart 2). As many of these countries have high economic growth rates, that is only right and proper. But it does mean that they, too, have a strong interest in a cure. And researchers would like to provide them with one.


The road to Berlin


A race is therefore on to work out how to flush the virus from its hiding places and get rid of it completely. Several clues suggest a cure may be possible. But no one knows which route will lead to it.


One of those routes passes through Timothy Brown. Mr Brown, pictured above, is known as the Berlin patient. He was living in that city in 2007 when he underwent radical treatment for leukaemia. This required the destruction of his immune system—the source of the cancer—and its replacement using stem cells transplanted from the bone marrow of a donor, which allowed him to grow a new (but alien) immune system.


Mr Brown did not just have leukaemia. He was also infected with HIV. So his doctor, with his permission, tried an experiment. The doctor searched for and found a donor who had a rare genetic mutation which confers immunity to HIV infection by disabling a protein on cell surfaces to which the virus attaches itself in order to gain entry to a cell.


After the transplant, the virus seemed to disappear from Mr Brown’s body. Traces of viral genes were found recently, but these may have been contamination, and in any case they did not amount to entire, working viruses. There is no disputing, however, that Mr Brown no longer needs drugs to stay healthy, and has not needed them for five years.


No one is suggesting immune-system transplants as a treatment for AIDS. They are far too dangerous and costly. The intriguing point about Mr Brown’s procedure is that it would have been expected to destroy directly only one of the hiding places of the virus: immune-system cells squirrelled away in a quiescent state as the system’s memory. (These allow it to recognise and respond to infections experienced in the past.) Other reservoirs, particularly certain brain cells, would not have been affected directly—and in Mr Brown’s case checking his brain to find out what is going on would be grossly unethical.


Clearly, it is dangerous to draw conclusions from a single example. But if quiescent memory cells are the main source of viral rebound, that would simplify the task of finding a cure. And many groups of researchers are trying to do just that, by waking up the memory cells so that ARVs can get at the virus within them.


Once such group, led by David Margolis of the University of North Carolina, uses an established anticancer drug called vorinostat as the wake-up call. This drug activates quiescent cells by tweaking the proteins that wrap their DNA. Dr Margolis’s latest results, announced to the conference and published simultaneously in Nature, suggest vorinostat does indeed awaken dormant memory cells, though the experiment did not ask whether that can in turn lead to the elimination of the virus.


Dr Margolis’s approach looks interesting. But it is not the only one on offer. A second, the so-called Visconti trial undertaken by France’s National Agency for Research on AIDS, studied people who had been put on ARVs immediately after they became infected. Some of these, the study found, become what are known as elite controllers.


An elite controller is an individual who is infected, but whose immune system seems able to suppress viral replication by itself. Elite controllers thus never develop the symptoms of AIDS. Natural cases of elite control are rare, but the Visconti trial (the name is a contraction of “Virological and immunological studies in controllers after treatment interruption”) seems to have found a way to create them artificially. Its dozen participants have lived without ARVs for an average of six years, having previously used them for an average of three. And the latest results from the study suggest the pattern of infection of their immune system closely resembles that seen in natural elite controllers.


Reasons to be cheerful


Amid all this scientific interest, however, the conference did not neglect the more immediate question of how the tools now available can be deployed. The watchword, borrowed from the jargon of drug delivery, is combination prevention.


The crucial trick with ARVs is to use several different treatments simultaneously, an approach known as combination therapy. Attacked from many directions, the virus cannot escape. A similar method is now being applied to preventing transmission. Three techniques, beyond the traditional (and successful) one of exhorting couples to use condoms, have now been demonstrated to work. Researchers are busy crunching data that will allow them to suggest what emphasis should be placed on which techniques in different parts of the world.


One technique, treatment-as-prevention, relies on the fact that ARVs themselves suppress transmission. A cross-continental study published last year showed that, when given to infected individuals whose sexual partners are uninfected, ARVs reduce by 96% the rate of transmission of the virus to the uninfected partner. Another study, published this July, showed that giving ARVs to the uninfected partner reduces their chances of becoming infected by 75%. These studies prove what might reasonably be suspected: that the smaller the amount of virus in someone’s body, the harder it is to pass it on; and that organising a hostile reception makes it hard for the virus to take hold.

方法一就是抑制疗法依赖由不同的抗病毒逆转类药物本身所起的作用能抑制艾滋病病毒的传播. 去年发表的跨洲研究表明当给一个其性伴侣没有感染艾滋病病毒的感染者使用多种抗病毒逆转类药物可以降低病毒传染给这个没有感染病毒的性伴侣,其有效率高达96%。而于今年7月发表的另一项研究表明采用给没有感染病毒者使用多种抗病毒逆转类药物会降低他们被感染病毒的机会,有效率高达75%。这些研究虽说可能还有理由表示怀疑不过却证明了某些人体内病毒量越少,病毒传播也就越难。刻意地去组合一个强有力的治疗方案会使病毒无法立足。

Treatment-as-prevention raises questions about how ARVs should be used in the future. At the moment, 8m people in poor and middle-income countries take them and the aim is to increase that to 15m. At that point, all those sick enough to warrant being treated would be under treatment. But a further 19m are infected. Prevailing opinion is that they need not be treated because their disease has not progressed to a point where it threatens their health. Yet if ARVs were used as preventatives, these people, too, would need to take them. Many would, to avoid infecting their lovers. But some might not want to. And for those who did the ARVs would have to be paid for. So the drug bill would go up.


The second approach uses ARVs to stop one very specific form of transmission: that between an infected mother and her child at birth, or during suckling. Using the latest drugs this is more than 95% effective, and it is easy to do because most pregnant women go to a doctor or a clinic before they give birth and can thus (with their permission) be tested for HIV.


The third technique is circumcision. Men’s foreskins are rich in immune-system cells, which are there to prevent the entry via the penis of infectious agents. Unfortunately, some of these cells are particularly susceptible to HIV infection. Removing the foreskin thus has a huge effect. It reduces, by about two-thirds, the risk of a man becoming infected. And follow-up studies suggest that with time this figure may rise to three-quarters.


In Africa, circumcision has, as it were, gone viral. The definitive studies showing it worked were published in 2006. After a slow start, hundreds of thousands of men have now had the snip. In 13 countries of eastern and southern Africa that are regarded by the World Health Organisation as being priority areas for the procedure, over half a million men were circumcised explicitly for AIDS protection between 2008 and 2010. The clinics can barely keep up, and several devices designed to simplify the process are now being tested.


The upshot of all this activity is a marked reduction in the rate of new infections, though sceptics point out that the fall began before ARV use and circumcision became widespread, and that the role of behavioural changes (including a greater willingness to use condoms) should thus not be underestimated.


Regardless of the cause, the graphs are all pointing in the right directions: ARV use is up; deaths and new infections are down. Soon, more people will be put on ARVs each year than die of the disease. That will be cause for celebration. AIDS is not yet beaten, and may be a long time in the beating. But if the will is there, then the means exist to do it.