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美找出骨髓细胞抵抗HIV感染的关键蛋白
2011年07月04日07:59 来源：《科技日报》 刘霞
本报讯 据美国物理学家组织网6月29日报道，美国科学家找到了细胞因子SAMHD1蛋白抑制骨髓细胞感染HIV（艾滋病病毒）的机制，新研究扩展了人们对艾滋病患者免疫系统如何对付HIV以及HIV如何逃避免疫反应的理解，从而找到阻止HIV感染或者阻止其在感染者体内复制的新疗法。相关研究发表在6月30日出版的《自然》杂志上。
骨髓细胞是提供抗原的白血细胞的一个子集，对身体抵抗病毒和其他病原体的免疫反应非常重要。凯斯西储大学医学院艾滋病研究中心研究员杰克·斯科沃斯基的研究团队和美国斯托瓦斯医学研究所的迈克尔·沃什本领导的团队合作发现，SAMHD1蛋白能感应到诸如巨噬细胞和树状细胞等骨髓细胞感染到HIV-1病毒（HIV分为1型和2型，1型是目前全球流行的主要毒株，2型目前只在西非流行）和其他相关的免疫缺陷病毒，并阻止病毒副本在这些细胞内的合成，从而抑制HIV病毒感染。
以前，科学家们一直认为，SAMHD1发生变异会引发一种名为AGS的症状，这种症状和先天病毒感染一样，要归咎于在病毒缺席时，免疫系统内干扰素的不适当诱导。因此，SAMHD1和其他引发AGS的细胞蛋白能摒弃细胞的核酸碎片，预防这种干扰素系统被不适当地激活。
现在，斯科沃斯基团队发现，除了能预防不适当的自身免疫反应发生之外，SAMHD1也能通过有效干预病毒核酸的产生从而抑制骨髓细胞感染HIV。
他们还发现，HIV-2和相关的免疫缺陷病毒（SIVsm/mac）能够通过使用它们编码的Vpx蛋白来干掉SAMHD1，从而越过骨髓细胞内的保护机制，使人感染病毒。然而，令人感兴趣的是，与HIV-1相比，诸如HIV-2等拥有Vpx的病毒更不容易引发疾病。斯科沃斯基表示，这可能是因为通过能在骨髓细胞内建立感染，HIV-2等病毒激起了比HIV-1更强烈的免疫反应。
斯科沃斯基表示，操纵SAMHD1的功能可能会让感染HIV-1患者对这种病毒产生更强烈的免疫反应。科学家们下一步将研究SAMHD1用来抑制HIV-1感染的分子路径。（刘霞）(科技日报)
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| 图示∶2011年5月正式出版的《中国特色医疗金鉴》登载的刘君主任及其机构事迹 |
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Bone marrow cells against the United States to identify key protein in HIV infection
At 07:59 on July 4, 2011 Source: "Technology Daily" Liu Xia
WASHINGTON According to the American physicist Organizations June 29, U.S. scientists found a cytokine SAMHD1 protein inhibits bone marrow cells infected with HIV (AIDS virus) mechanism, a new study on the expansion of people's immune system how to deal with AIDS patients and HIV HIV to evade the immune response to understand how to prevent HIV infection found in the infected person or prevent the body copy of the new therapy. Research published in the June 30 issue of "Nature" magazine.
Bone marrow cells are white blood cells to provide antigen in a subset of the body against viruses and other pathogens, the immune response is very important. Case Western Reserve University School of Medicine AIDS Research Center Jakes Coward Chomsky's research team and the United States Stowers Institute for Medical Research Michael Washburn led team found that, SAMHD1 protein senses, such as macrophages and dendritic cells such as bone marrow cells infected with HIV-1 virus (HIV divided into type 1 and type 2, type 1 is a major global epidemic strain, type 2 epidemic in West Africa is currently only), and other related immune deficiency virus, copies of the virus and prevent the synthesis of these cells to inhibit HIV infection.
Previously, scientists assumed that, SAMHD1 mutate and trigger the symptoms called AGS, congenital viral infections such as symptoms and should be attributed to the absence of the virus, the immune system, inappropriate induction of interferon. Therefore, SAMHD1 and other cellular proteins can lead to abandon the AGS cell DNA fragmentation, prevent the interferon system is inappropriately activated.
Now, Scott Jaworski team found that, in addition to preventing inappropriate autoimmune reaction in addition, SAMHD1 also through effective intervention to inhibit the production of viral nucleic acid bone marrow cells infected with HIV.
They also found that, HIV-2 and related immunodeficiency virus (SIVsm / mac) can be encoded by using them to kill the Vpx protein SAMHD1, bone marrow cells to cross the protective mechanism, people infected with the virus. However, it is interesting that, compared with HIV-1, such as HIV-2 virus has Vpx less likely to cause illness. Scott Jaworski said that this may be because in the bone marrow cells through the establishment of infection, HIV-2 and other viruses than HIV-1 provoked a stronger immune response.
Scott Jaworski said manipulation SAMHD1 function may make patients infected with HIV-1 virus produces a stronger immune response. Scientists will study SAMHD1 next to inhibit HIV-1 infection of molecular pathways. (Liu Xia) (Technology News)
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