最新一項(xiàng)研究發(fā)現(xiàn),，丙肝蛋白中的一個(gè)片段可以在細(xì)胞培養(yǎng)中防止HIV感染,，預(yù)示著一種新的對(duì)抗HIV病毒武器的出現(xiàn),。Philippe Gallay所在的研究小組發(fā)現(xiàn),，C5A肽可以打亂HIV粒子并摧毀他們的傳染性,。這種肽是丙肝病毒錨蛋白的一部分,，之前的研究發(fā)現(xiàn)它對(duì)丙肝病毒有殺滅作用。在這項(xiàng)研究中,，C5A可以摧毀會(huì)傳染的HIV粒子,，從而阻止HIV進(jìn)入其首要的目標(biāo)細(xì)胞——CD4+T細(xì)胞、巨噬細(xì)胞和樹狀細(xì)胞——同時(shí)不破壞這些細(xì)胞的細(xì)胞膜,。
研究人員強(qiáng)調(diào),，這一抗病毒機(jī)制不同于其它那些基于蛋白質(zhì)的、阻止HIV接受體互動(dòng)的抗HIV藥物,。這種肽還可以防止HIV病毒在形成生殖器膜的細(xì)胞間轉(zhuǎn)移,，并阻止病毒到達(dá)膜下的細(xì)胞目標(biāo)。研究人員相信,，如果進(jìn)一步的研究表明這種肽對(duì)人體同樣安全,，那么C5A就可能可以作為一種預(yù)防HIV的抗微生物劑，擁有治療價(jià)值,。
相關(guān)論文3月31日在線發(fā)表于美國(guó)《國(guó)家科學(xué)院院刊》（PNAS）上,。（來(lái)源：EurekAlert!中文版）
生物谷推薦原始出處：
（PNAS）， doi：10.1073/pnas.0801388105,，Michael D. Bobardt,，Philippe A. Gallay
Hepatitis C virus NS5A anchor peptide disrupts human immunodeficiency virus
Michael D. Bobardt*, Guofeng Cheng, Lot de Witte, Suganya Selvarajah*, Udayan Chatterji*, Brigitte E. Sanders-Beer, Teunis B. H. Geijtenbeek, Francis V. Chisari,¶, and Philippe A. Gallay*,¶
Departments of *Immunology and Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037; Department of Molecular Cell Biology and Immunology, VU University Medical Center, van de Boechorststraat 7, 1081 BT, Amsterdam, The Netherlands; and BIOQUAL, Inc., 9600 Medical Center Drive, Rockville, MD 20850
Contributed by Francis V. Chisari, February 12, 2008 (sent for review December 7, 2007)
Abstract
In the absence of an effective vaccine, there is an urgent need for safe and effective antiviral agents to prevent transmission of HIV. Here, we report that an amphipathic -helical peptide derived from the hepatitis C virus NS5A anchor domain (designated C5A in this article) that has been shown to be virocidal for the hepatitis C virus (HCV) also has potent antiviral activity against HIV. C5A exhibits a broad range of antiviral activity against HIV isolates, and it prevents infection of the three in vivo targets of HIV: CD4+ T lymphocytes, macrophages, and dendritic cells by disrupting the integrity of the viral membrane and capsid core while preserving the integrity of host membranes. C5A can interrupt an ongoing T cell infection, and it can prevent transmigration of HIV through primary genital epithelial cells, infection of mucosal target cells and transfer from dendritic cells to T cells ex vivo, justifying future experiments to determine whether C5A can prevent HIV transmission in vivo.
