【TED】为什么艾滋病如此难以治愈?

中英文稿
2008 年,难以置信的事情发生了: 一名HIV患者被成功治愈 在超过七千万HIV病例中,这是第一例, 目前为止也是最后一例 我们无法确切的知道他是如何被治好的 我们可以治愈很多疾病,比如疟疾与丙肝 但是我们为何不能治愈HIV? 首先,让我们来看HIV病毒是如何感染人类 以及如何发展成为艾滋病
HIV病毒通过体液交换传播 无保护的性行为和污染的针头是传播的主要原因 幸运的是,HIV 无法通过空气、水或者接触传播 任何年纪,性取向,性别和种族的个体 都有可能感染HIV
一旦进入人体,HIV病毒便开始感染免疫系统的细胞 它专门攻击辅助型T细胞 这是一种帮助人体抵抗细菌和真菌感染的细胞 HIV 是逆转录病毒 它可以将自己的基因编码写入被感染细胞的基因组 指派他们复制更多的病毒
在HIV感染初期 病毒在辅助性T细胞中复制 在这个过程中破坏了许多T细胞 在这个阶段,患者通常有类似流感的症状 但不会有生命危险 在几个月甚至几年的一段时期内 患者可能看起来很健康 但病毒持续复制,同时破坏T细胞 当T细胞数目过低 患者将处于致死性感染的危险中 这种感染在健康的免疫系统中是可以被抵御的 HIV感染的这个阶段被称作艾滋病
好消息是已经有有效的药物 能够控制HIV病毒水平, 并防止T细胞数目过低, 从而避免发展成为艾滋病 如果进行抗逆转录病毒治疗, 大部分HIV阳性的病人能够继续正常生活 而且也会减少对其他人的感染
但目前有两个难点 第一,HIV阳性病人在有生之年 必须一直服药 如果停止,HIV会恶化
那么,这些药物是如何起作用的? 最常用的那些临床药物可以阻止病毒的基因 复制并合并入宿主细胞DNA 其他的药物可以阻止病毒的变异和组装 使得HIV病毒不能感染体内其他细胞
但是HIV病毒会藏在目前药物无法到达的地方: 健康T细胞的DNA中 大部分T细胞被HIV传染后迅速死亡 但是很小的一部分 被用作构建更多HIV病毒的场所,会处于休眠 有时甚至好几年 因此,即使我们能够清除感染人体的每一个HIV病毒 一个这样的T细胞就能激活并且重新传播病毒
另一个难点是,并不是世界上的所有人都能获得 这些能够挽救他们生命的药物 在撒哈拉以南非洲, 这个地区占全球艾滋病患者的70%以上 2012年,仅有三个HIV阳性患者接受抗逆转录病毒治疗 这个问题很难解决 政治,经济,文化的障碍 使得有效的预防和治疗变得困难 即使是在美国,每年HIV夺去超过10000人的生命
但是依然有希望 研究人员比以往任何时候都接近发展出真正的治疗方法 一项研究涉及 使用一种药物激活隐含HIV遗传信息的所有细胞 这将破坏这些细胞并且将病毒暴露出来 接着我们现有的药物就可以起作用了 另外一种是使用基因工具 将HIV的DNA从细胞基因组剪切下来
尽管七千万人中仅有一例治愈 但是一个总比没有好 我们现在清楚治疗还是有可能的 这告诉我们将需要什么去击败HIV
In 2008, something incredible happened: a man was cured of HIV. In over 70 million HIV cases, that was a first and, so far, a last. We don't yet understand exactly how he was cured. We can cure people of various diseases, such as malaria and hepatitis C, so why can't we cure HIV? Well, first let's examine how HIV infects people and progresses into AIDS.
HIV spreads through exchanges of bodily fluids. Unprotected sex and contaminated needles are the leading cause of transmission. It, fortunately, cannot spread through air, water, or casual contact. Individuals of any age, sexual orientation, gender and race can contract HIV.
Once inside the body, HIV infects cells that are part of the immune system. It particularly targets helper T cells, which help defend the body against bacterial and fungal infections. HIV is a retrovirus, which means it can write its genetic code into the genome of infected cells, co-opting them into making more copies of itself.
During the first stage of HIV infection, the virus replicates within helper T cells, destroying many of them in the process. During this stage, patients often experience flu-like symptoms, but are typically not yet in mortal danger. However, for a period ranging from a few months to several years, during which time the patient may look and feel completely healthy, the virus continues to replicate and destroy T cells. When T cell counts drop too low, patients are in serious danger of contracting deadly infections that healthy immune systems can normally handle. This stage of HIV infection is known as AIDS.
The good news is there are drugs that are highly effective at managing levels of HIV and preventing T cell counts from getting low enough for the disease to progress to AIDS. With antiretroviral therapy, most HIV-positive people can expect to live long and healthy lives, and are much less likely to infect others.
However, there are two major catches. One is that HIV-positive patients must keep taking their drugs for the rest of their lives. Without them, the virus can make a deadly comeback.
So, how do these drugs work? The most commonly prescribed ones prevent the viral genome from being copied and incorporated into a host cell's DNA. Other drugs prevent the virus from maturing or assembling, causing HIV to be unable to infect new cells in the body.
But HIV hides out somewhere our current drugs cannot reach it: inside the DNA of healthy T cells. Most T cells die shortly after being infected with HIV. But in a tiny percentage, the instructions for building more HIV viruses lies dormant, sometimes for years. So even if we could wipe out every HIV virus from an infected person's body, one of those T cells could activate and start spreading the virus again.
The other major catch is that not everyone in the world has access to the therapies that could save their lives. In Sub-Saharan Africa, which accounts for over 70% of HIV patients worldwide, antiretrovirals reached only about one in three HIV-positive patients in 2012. There is no easy answer to this problem. A mix of political, economic and cultural barriers makes effective prevention and treatment difficult. And even in the U.S., HIV still claims more than 10,000 lives per year.
However, there is ample cause for hope. Researchers may be closer than ever to developing a true cure. One research approach involves using a drug to activate all cells harboring the HIV genetic information. This would both destroy those cells and flush the virus out into the open, where our current drugs are effective. Another is looking to use genetic tools to cut the HIV DNA out of cells genomes altogether.
And while one cure out of 70 million cases may seem like terrible odds, one is immeasurably better than zero. We now know that a cure is possible, and that may give us what we need to beat HIV for good.