[日期：2006-02-14]
廣東發現30例長期不感染艾滋者 可能有抗艾基因
首屆中國東南部艾滋病國際學術研討會昨發表最新觀點
科學家最新發現：人體內HIV最為集中的是腸道而不是血液，因此肛交容易感染。
另外發現一種用於治療哮喘病的中藥可能對防艾滋病毒慢性感染有效。
記者昨日從在暨南大學舉行的第一屆中國東南部艾滋病國際學術研討會上獲悉，目前廣東已經找到了30例「長期暴露」卻未感染HIV的個案，科學家們將研究他們身上可能存在的「抗艾基因」，而中藥治療艾滋病也有了利好消息。此外，最新公佈的研究成果顛覆了多年的主流觀點：腸道中艾滋病毒比血液更集中。
腸道病毒密度最高肛交易染艾滋
聯合國艾滋病總署專員、美國華盛頓大學教授朱托夫、中華醫學會會長鐘南山院士等知名學者出席了昨日的國際學術研討會。記者從會上獲悉，目前全球的艾滋病基礎研究有了突破性的發現，多年來科學界一直以為血液裡攜帶了最大量的HIV，但科學家最新研究發現，人體內HIV最為集中的病灶是腸道,血液內的病毒載量僅佔2％~5％，近80％的HIV都在腸道組織內，且對免疫系統的傷害在感染後第一二周最為嚴重。「HIV進入人體攻佔的主要目標是淋巴細胞，腸道是淋巴組織、淋巴最豐富的地方，所以吸引了非常多的HIV。」專家們說：「這就能解釋男同性戀感染艾滋病的風險很高，因為肛交直接接觸HIV最密集的區域，一旦有傷口破損，高密度的病毒就可能進入健康人的體內，造成感染。」非洲的一項治療也佐證了這一發現，當地對艾滋病兒童施於抗菌素，抑制腸道炎症的發展，降低了HIV的繁殖速度，使得病孩的死亡率下降了20％。專家們興奮地表示，這提示了腸道是治療艾滋病的重要靶點。他們也再三強調，艾滋病毒並不經消化道傳染，只是病毒進入體內後容易在腸道內集合，目前已知的仍是性交、靜脈注射、母嬰傳播三種途徑。
廣東找到30例長期不感染者
從去年開始，朱托夫教授就和暨南大學艾滋病基因與疫苗研究開發中心聯合攻關，尋找中國人的抗艾滋病基因，昨日記者瞭解到了最新進展。
一年多來，研究組從廣州市第八人民醫院，廣州市、深圳市疾控中心等單位獲取了300多份HIV陽性血樣，尋訪到其中的80位HIV攜帶者、艾滋病人及他們的生活伴侶，其中有30例長期反覆進行無保護性接觸者的性伴侶沒有感染艾滋病。30例中有兩例符合基因變異的發現，另外28例不感染的原因還在研究中，專家認為這可能和機體本身免疫力、進入人體病毒數量等因素相關。研究組還採集了1000多份正常人血液樣本，對照尋找變異基因發生的概率，目前已經檢測了半數。
中藥對抑制HIV呈現作用
中國首個進入人體實驗的艾滋病疫苗此前一直備受關注，朱托夫教授也是這項科研項目的參與專家。據介紹，現在廣西進行的疫苗人體實驗還處於毒性試驗階段，可以肯定疫苗無毒性，免疫效果試驗還要在後面進一步研究。朱托夫稱，疫苗的研究是必須的，但是困難重重，進行到三期研究以後的有效疫苗有實際意義，目前仍還有很長一段路要走。
暨南大學組織移植與免疫研究中心主任曾耀英介紹中藥對抗「艾」作用不容忽視，正在進行的一項研究表明，一種用於治療哮喘病的中藥可能對艾滋病毒慢性感染有效。這種注射液對人的靜止T細胞具有弱的活化作用和抗凋亡的作用，而對人的活化T細胞具有較強抑製作用，抑制了T細胞的活性，就能有效阻斷HIV進入淋巴組織。2年前第一期在河南已經完成30例試驗，現在正在雲南進行第二期，案例增加到100例，效果較為理想。
名詞解釋
「長期暴露不感染者」
美國華盛頓大學朱托夫實驗室曾對美國1萬名同性戀者進行跟蹤研究，結果發現有近100人雖然和艾滋病人長期保持無安全措施的性關係，但始終沒有感染HIV，這一特殊人群被定義為「長期暴露不感染者」，研究發現3%的人具有DC-SIGN變異基因，他們終身不會感染HIV；30%的人具有DC-SIGN（R）變異基因，感染HIV的機會是普通人的1／19，很可能是這個變異的基因導致他們有天生屏蔽HIV的功能。 （記者 姜永濤 通訊員 溫志勤）
Cell Protein Found That Literally Nips HIV In The Bud
ScienceDaily (Jan. 14, 2008) — UCLA researchers have found that a key protein in the body’s dendritic cells can stop the virus that causes AIDS from ”budding” -- part of the virus’ life cycle that is crucial to its ability to replicate and infect other cells.
”If we can block virus generation, then we can control the disease,” said lead author Shen Pang, associate professor in the division of oral biology and medicine at the UCLA School of Dentistry and a member of the UCLA AIDS Institute.
Dendritic cells are specialized white blood cells in the skin, mucosa and lymph nodes that kick-start a primary immune response to foreign invaders by activating lymphocytes, including the T cells that HIV targets. Though dendritic cells can be infected with HIV -- and indeed play a crucial role in transmitting the virus to T cells -- studies have shown that viral generation from these cells is nearly a hundred times lower than from infected T cells, indicating that the cells may possess some inhibiting property.
Pang hypothesized that DC-SIGN, a protein expressed in dendritic cells, may be responsible for such inhibition. He and his colleagues found that DC-SIGN and a related protein, DC-SIGNR, both demonstrated 95 percent to 99.5 percent inhibition of viral production from host cells.
Very few cells are infected when HIV first enters the human body, but the virus rapidly creates new copies of itself, which in turn infect more cells. To achieve this, the virus, after infecting a cell, sends envelopes of protein to the cell’s membrane. The viral genomes then combine with viral structural proteins and move into these envelopes. The envelopes bubble, or bud, outward, releasing viral particles that will infect more cells and start new viral life cycles.
According to the researchers, DC-SIGN appears to block HIV generation by efficiently neutralizing an HIV glycoprotein on the surface of the HIV envelope known as gp120, a key to viral infection. In such cases, while some viral particles may still be released from the infected dendritic cells, the lack of gp120 in their envelopes means they are not infectious to CD4-positive T-lymphocytes and macrophages. In other words, these viral particles have been rendered uninfectious.
Current methods to interrupt the life cycle of the virus are limited because they generally target HIV at the stages of viral entry, reverse transcription and post-translational protein cleavages. Once the virus passes through these stages, treatment fails. The UCLA researchers, therefore, focused on halting the virus’ generation at different stages in its life cycle.
”The strong inhibition of viral production by DC-SIGN suggests the possibility of using this protein for treatment of HIV-infected patients,” the researchers write. ”Expression of this protein in various CD4-positive cells should inhibit viral production from infected cells. Because it can also enhance the immune response, DC-SIGN is expected to be useful for in vivo studies for developing an HIV vaccine.”
The study, scheduled for publication in the April issue of the Federation of American Societies for Experimental Biology’s FASEB Journal and may be available online at
http://www.fasebj.org/cgi/rapidpdf/fj.07-9443comv3.pdf. Pang’s co-author is Qiuwei Wang, a postgraduate researcher in the division of oral biology and medicine at the UCLA School of Dentistry.
This study was supported by the UCLA AIDS Institute, the UCLA School of Dentistry and a grant from the National Institutes of Health.
Adapted from materials provided by University of California - Los Angeles, via EurekAlert!, a service of AAAS.
