耶鲁大学的研究人员开发了一种分子，该分子能够加强机体对HIV和HIV感染的细胞的免疫应答，此外还包括前列腺癌细胞。这项研究结果发布在Journal of the American Chemical Society的在线版本上，或能有助于开发新的疾病疗法。
这种分子分别叫ARM-H（靶向定位HIV），和ARM-P（靶向定位前列腺癌细胞）。在HIV感染的细胞中，该分子能够同时绑定到已经存在于血液中的抗体以及HIV蛋白上。通过抗体包围病原菌，这个分子能够对病原菌进行标记，激发机体自身的免疫系统。ARM-H通过绑定病毒外围的蛋白，同样也可以保护健康的细胞，使其免受影响。
研究人员不是通过直接杀死病原菌，而是通过免疫系统。这类分子能够调控我们的免疫系统，使其去做一些平时不会做的事情。David Spiegel教授介绍说。
由于HIV和癌症能够躲避机体的免疫系统，而且这两种疾病的疗法和疫苗都是比较难开发的。目前对于HIV和前列腺癌的疗法，主要包括抗病毒药，辐射和化疗，但通常会伴随严重的副作用。然而一些可行的抗体药物又很难去大量生产，而且代价昂贵，同样的，其本身可能也有严重的副作用。
研究小组发现，ARM-H和ARM-P分子的结构简单，生产成本较低，从理论上说是能够以药片的形式生产的。Spiegel介绍说，由于它们不会靶向定位机体中一些重要的生物学过程，所以副作用可能相对较小。
这项研究将有助于开发一种治疗HIV和前列腺癌的全新方法，对人类健康来说是非常重要的。（生物谷Bioon.com）
生物谷推荐原始出处：
J. Am. Chem. Soc., 2009, 131 (45), pp 16392–16394 DOI: 10.1021/ja9057647
An Antibody-Recruiting Small Molecule That Targets HIV gp120
Christopher G. Parker?, Robert A. Domaoal?, Karen S. Anderson? and David A. Spiegel*??
Department of Chemistry, Yale University, 225 Prospect Street, P.O. Box 208107, New Haven, Connecticut 06520-8107, and Department of Pharmacology, Yale University School of Medicine, 333 Cedar Street, SHM B350B, New Haven, Connecticut 06520
HIV/AIDS is a global pandemic for which new treatment strategies are desperately needed. We have designed a novel small molecule, designated as ARM-H, that has the potential to interfere with HIV survival through two mechanisms: (1) by recruiting antibodies to gp120-expressing virus particles and infected human cells, thus enhancing their uptake and destruction by the human immune system, and (2) by binding the viral glycoprotein gp120, inhibiting its interaction with the human protein CD4 and preventing virus entry. Here we demonstrate that ARM-H is capable of simultaneously binding gp120, a component of the Env surface viral glycoprotein (found on the surface of both HIV and virus-infected cells) and anti-2,4-dinitrophenyl antibodies (already present in the human bloodstream). The ternary complex formed between the antibody, ARM-H, and gp120 is immunologically active and leads to the complement-mediated destruction of Env-expressing cells. Furthermore, ARM-H prevents virus entry into human T-cells and should therefore be capable of inhibiting virus replication through two mutually reinforcing mechanisms (inhibition of virus entry and antibody-mediated killing). These studies demonstrate the viable anti-HIV activity of antibody-recruiting small molecules and have the potential to initiate novel paradigms in HIV treatment.
