2008年文登學校春季詞匯班精彩文篇推薦(十)

第十篇

An AIDS Mystery Solved

(1) About 15 years ago, a well-meaning man donated blood to the Red Cross in Sydney, Australia, not knowing he has been exposed to HIV-1, the virus that causes AIDS. Much later, public-health officials learned that some of the people who got transfusions? containing his blood had become infected with the same virus; presumably they were almost sure to die. But as six years stretched to 10, then to 14, the anxiety of health officials gave way to astonishment. Although two of the recipients have died from other causes, not one of the seven people known to have received transfusions of the man’s contaminated blood has come down with AIDS. More telling still, the donor, a sexually active homosexual, is also healthy. In fact his immune system remains as robust as if he had never tangled with HIV at all. What could explain such unexpected good fortune?

(2) A team of Australian scientists has finally solved the mystery. The virus that the donor contracted and then passed on, the team reported last week in the journal Science. contains flaws in its genetic script that appear to have rendered it innocuous?. “Not only have the recipients and the donor not progressed to disease for 15 years,” marvels molecular biologist Nicholas Deacon of Australia’s Macfarlane Burnet Centre for Medical Re-search, “but the prediction is that they never will.” Deacon speculates that this “impotent” HIV may even be a natural inoculant? that protects its carriers against more virulent strains? of the virus, much as infection with cowpox warded off smallpox in 18th-century milkmaids.

(3) If this ______ proves right, it will mark a milestone in the battle to contain the late-20th century’s most ter-rible epidemic. For in addition to explaining why this small group of people infected with HIV has not become sick, the discovery of a viral strain that works like a vaccine would have far-reaching implications. “What these results suggest,” says Dr. Barney Graham of Tennessee’s Vanderbilt University, “is that HIV is vulnerable and that it is possible to stimulate effective immunity against it.”

(4) The strain of HIV that popped up? in Sydney intrigues scientists because it contains striking abnormalities in a gene that is believed to stimulate viral duplication. In fact, the virus is missing so much of this particular gene — known as nef, for negative factor — that it is hard to imagine how the gene could perform any useful function. And sure enough, while the Sydney virus retains the ability to infect T cells — white blood cells that are critical to the immune system’s ability to ward off infection — it makes so few copies of itself that the most powerful molecular tools can barely detect its presence. Some of the infected Australians, for example, were found to carry as few as one or two copies of the virus for every 100000 T cells. People with AIDS, by contrast, are burdened with viral loads thousands of times higher.

(5) At the very least, the nef gene offers an attractive target for drug developers. If its activity can be blocked, suggests Deacon, researchers might be able to hold the progression of disease at bay, even in people who have developed full-blown AIDS. The need for better AIDS-fighting drugs was underscored last week by the actions of a U.S. Food and Drug Administration advisory panel, which recommended speedy approval of two new AIDS drugs, including the first of a new class of compounds called protease? inhibitors?. Although FDA commissioner David Kessler was quick to praise the new drugs, neither medication can prevent or cure AIDS once it has taken hold.

(6) What scientists really want is a vaccine that can prevent infection altogether. And that’s what makes the Sydney virus so promising — and so controversial. Could HIV itself, stripped of nef and adjacent sections of genetic material, provide the basis for such a vaccine, as Deacon and his colleagues cautiously suggest? Ongo-ing work on SIV, the simian? immunodeficiency virus that causes an AIDS-like illness in monkeys, indicates that this might be less far-fetched than it sounds. Ronald Desrosiers at the New England Regional Primate Re-search Center has demonstrated that when the nef gene is removed from SIV, the virus no longer has the power to make monkeys sick. Moreover, monkeys inoculated? with the nef free SIV developed marked resistance to the more virulent strain.

(7) But few scientists are enthusiastic about testing the proposition by injecting HIV — however weakened — into millions of people who have never been infected. After all, they note, HIV is a retrovirus?, a class of infec-tious agents known for their alarming ability to integrate their own genes into the DNA of the cells they infect. Thus once it takes effect, a retrovirus infection — unlike those of viruses that cause measles, smallpox and any number of others diseases — is permanent. While some retroviruses are benign, others can strike without warn-ing. Some remain hidden for years, only to trigger disease late in life when the immune system starts to de-crease.

(8) This makes vaccine development extremely risky. A weakened strain of SIV that protected adult monkeys, for example, looked safe until researchers at the Dana Farber Cancer Institute in Boston showed that newborn monkeys with immature immune systems did not respond as healthy adults do. All the young primates, in fact, developed the very disease the weakened virus was supposed to prevent. For this and a host of other reasons, most AIDS researchers argue that the only prudent strategy is to concoct? a hybrid? vaccine, putting the key features of a disabled AIDS virus into something more benign than a retrovirus. Among the leading candidates: the vaccinia virus that successfully wiped out smallpox.

(9) A handful of researchers, however, argue that the more dangerous retroviral vaccine should not be written off prematurely. Desrosiers, for one, believes the situation in parts of the developing world (where the chance of HIV infection may reach 40% among sexually active adults) has become so desperate that a retroviral vaccine may be worth the ______. A live vaccine made from HIV, he maintains, can be made safer by removing not just the nef gene but several others as well. Desrosiers has found that he can cripple HIV by chemically deleting four of its nine known genes and still get a virus that replicates, at least in chimpanzees.

(10) At present, concerns about safety are so overwhelming that effors to develop a live retroviral vaccine are unlikely to win much support. But that could change as studies of long-term survivors — that small, charmed circle of people who have been infected with the AIDS virus but have remained disease-free — provide new in-sights into the weaknesses of the viral enemy and the untapped strengths of its human targets. “These individu-als,” observes Dr. Warner Greene, director of the Gladstone Institute of Virology and Immunology in San Fran-cisco, “are natural experiments, and they hold a great secret that we are still trying to decipher?.” Indeed, it is entirely possible that the eight Australians who have caused such a stir will be cited by medical texts as the first people on the planet to be successfully, if accidentally, vaccinated against the AIDS virus — a virus that until now has seemed all but invincible.

【參考譯文】: 艾滋之謎揭曉

(1) 大約在15年前，澳大利亞悉尼有一位人士好心向紅十字會捐血，不知道自己已感染HIV-1型——這是造成艾滋病的病毒。多年以后，公共衛生官員發現，有些接受他血液輸血的人，也受到病毒感染。這些人應該是難逃死亡的噩運。可是6年、10年、14年過去了，衛生官員的焦慮變為驚奇。雖然其中有兩個人因其他原因死亡，可是接受遭污染血液輸血的這7個人當中，沒有一個人罹患艾滋病。更引人注目的是，那位捐血人——一個有性行為的同性戀者——仍然活得好好的。他的免疫系統十分強壯，就像從沒染上HIV一樣。這種意外的好運要如何解釋？

(2) 一批澳大利亞科學家終于解開了謎團。他們在上周的《科學》期刊發表報告指出：這位捐血人染上然后傳出去的病毒，基因結構有缺陷，可能因此變成無害。澳大利亞麥法蘭? 伯奈特醫學研究中心的分子生物學家迪肯嘖嘖稱奇：“捐血人與輸血人不僅15年來沒有發病，而且應該永遠不會發病。”迪肯大膽假設這種無能的HIV甚至可能是天然的疫苗，可以保護帶原者不受更厲害的病毒品種侵襲，就好像18世紀擠牛奶的女工感染牛痘之后就能抵抗天花一樣。

(3) 如果這個預感成真，那么在圍堵20世紀末比較可怕的傳染病的戰斗上，要立下一座里程碑。因為，發現一種具有疫苗功能的病毒品種，不僅能解釋這一小群受到HIV感染的人何以不發病，還具有更深遠的涵義。田納西州范德堡大學的格雷姆博士說：“這些結果暗示HIV也有弱點，也表示有可能刺激免疫系統來有效地對抗它。”

(4)在悉尼發現的這種HIV品種，引起科學家高度的頭趣，因為它有一個基因嚴重異常。一般認為這是刺激病毒去復制自我的基因。這種病毒在這個叫做“否因”（代表否定因素）的基因中大部分殘缺不全，很難想象這個基因能產生什么作用。果然，這種悉尼病毒雖然有能力感染T細胞（免疫系統對抗感染時比較關鍵的白血球細胞），可是復制的能力極差，連比較強大的分子工具也很難偵測到它的存在。就拿受到感染的這些澳大利亞人來說，其中有些人體內每10萬個T細胞才有一二個病毒。相反的，艾滋病患者則要承擔高幾千倍的病毒量。

(5)“否因”基因比較低限度對制藥公司是很大的誘惑。迪肯認為，假如能夠阻斷這種基因的活動，研究人員就有可能阻止病情的進展，就算是已經全面發作的艾滋病病人也一樣有用。對更好的艾滋藥物需求十分殷切，這由美國食品藥物管理局（FDA）顧問小組上周的一項行動可以看出。這個小組建議盡快批準兩種艾滋新藥，包括一類全新的化合物，稱為蛋白酶抑制劑。FDA局長戴維? 凱斯勒迅速贊揚這些新藥，可是這兩種藥都無法預防艾滋病，在感染艾滋病毒后也無法治愈。

(6)科學家真正想要的是能完全預防感染的疫苗，所以悉尼病毒才被寄以厚望，也才會引起爭議。HIV病毒除去“否因”與鄰近的一些基因物質后，是否真如迪肯和他的同僚審慎暗示的一樣，可以作為艾滋病疫苗的基礎？這個構想聽來很牽強，但是目前對猿猴免疫不全病毒（SIV，造成猿猴罹患類似艾滋病的病毒）所做的研究顯示并非毫無根據。新英格蘭區靈長類研究中心的戴斯羅士已經證明，從SIV中除去“否因”基因后，病毒就無法使猿猴發病。而且，猿猴接種過已去除“否因”的SIV后，會發展出明顯的抵抗力，可以抵抗毒性強的SIV品種。

(7) 但是沒有幾個科學家熱衷于檢驗這個構想——在幾百萬個沒有感染過艾滋病的人身上注射HIV（不論削弱到什么程度）。科學家指出，畢竟HIV是逆轉錄酶病毒。這種傳染媒介原以一種可怕的能力著稱：能把本身的基因合并到受感染細胞的DNA內。所以一旦感染上逆轉錄酶病毒，就永遠擺脫不掉。這和造成麻疹，天花以及其他許多疾病的病毒都不一樣。有些種類的逆轉錄酶病毒是良性的，也有一些發作起來毫無征兆。有些則是潛伏多年，直到人進入老年，免疫系統功能衰退時才發病。

(8)因此，開發疫苗的風險極大。舉例來說，有一種削弱了的SIV病毒可以保護成年猴子，似乎也很安全。可是波士頓戴納? 法柏癌癥研究所的人員后來發現，初生的小猴，免疫系統尚不成熟，反應也和健康的成猴不同。這些小猴全部發生了當初用弱性疫苗所要預防的疾病。因為這個案例，再加上許多別的原因，艾滋病研究人員大多主張，唯一較謹慎的策略是調配出混種病毒，也就是把弱化艾滋病毒的主要特征放到比逆轉錄酶病毒良性的病毒中。比較理想的對象包括當年成功撲滅天花的疫苗病毒。

(9)也有少數幾位研究人員，主張不能斷然否定掉危險性較高的逆轉錄酶病毒疫苗。戴斯羅士就認為，某些發展中國家的情況十分危急（有性行為的成年人感染HIV的比例可以達到40% ），值得冒險一試逆轉錄酶病毒疫苗。他主張可以把HIV病毒中的幾種基因與“否因”一并移除，就能增加活疫苗的安全性。戴斯羅士發現，可以用化學方式刪除HIV9種已知基因中的4種，破壞掉HIV的力量，制造出來的病毒仍然會復制——至少在黑猩猩身上可以。

(10)目前對于安全性的關注高過一切，要想培養活的逆轉錄酶病毒疫苗，不大可能得到太多人支持。可是情況也可能改變。對艾滋病長期生存者的研究（也就是那一小群感染到艾滋病毒卻一直沒有發病的幸運者），可以讓我們更深入了解病毒的弱點與人類尚未發現的力量。舊金山格萊斯頓病毒與免疫研究所所長格林博士表示：“這幾個人是大自然的實驗，手中握有一大奧秘，還有待破謎。”確實，這8名引起軒然大波的澳大利亞人，很有可能被醫學文獻列為地球上比較早成功地（盡管是意外地）接受艾滋病毒免疫注射的人——雖然到目前為止艾滋病毒好像還是所向無敵。