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首页> 外文期刊>The Mount Sinai journal of medicine >Chemokine (C-C Motif) Receptor 5 Entry Inhibitors: New Class of Drugs for Acquired Immune Deficiency Syndrome
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Chemokine (C-C Motif) Receptor 5 Entry Inhibitors: New Class of Drugs for Acquired Immune Deficiency Syndrome

机译:趋化因子(C-C母题)受体5进入抑制剂:获得性免疫缺陷综合症的新型药物

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摘要

Recently, a new anti-acquired immune deficiency syndrome (AIDS) drug called maraviroc was shown to be effective against human immunodeficiency virus (HIV) in patients who did not respond well to other antiretroviral therapies. Maraviroc represents a novel class of drugs called chemokine (C-C motif) receptor 5 (CCR5) entry inhibitors. Unlike other antiretrovirals currently in use, it targets a human cell surface protein to which HIV attaches. If it is approved by the Food and Drug Administration, maraviroc would be the first drug against AIDS that targets the human host cell rather than the virus itself. HIV infection commences with the binding of viral envelope proteins to CD-4 receptors on a host immune cell. Although CD-4 binding is required, it is not sufficient in itself for HIV infection. In order to gain entry into the cell, HIV must also bind a host coreceptor, either CCR5 or chemokine (C-X-C motif) receptor 4 (CXCR4). Interactions between HIV envelope proteins and host cell receptors trigger the fusion of the viral lipid membrane with that of the host cell.
机译:最近,一种新的抗后天免疫缺陷综合症(AIDS)药物maraviroc已被证明在对其他抗逆转录病毒疗法反应不佳的患者中可有效抵抗人类免疫缺陷病毒(HIV)。 Maraviroc代表了一类新型药物,称为趋化因子(C-C主题)受体5(CCR5)进入抑制剂。与目前使用的其他抗逆转录病毒药物不同,它靶向HIV附着的人类细胞表面蛋白。如果获得食品和药物管理局(FDA)的批准,马拉维罗克将成为针对人类宿主细胞而非病毒本身的首个抗艾滋病药物。 HIV感染始于病毒包膜蛋白与宿主免疫细胞上CD-4受体的结合。尽管需要CD-4结合,但它本身不足以感染HIV。为了进入细胞,HIV还必须结合宿主共受体,即CCR5或趋化因子(C-X-C基序)受体4(CXCR4)。 HIV包膜蛋白与宿主细胞受体之间的相互作用触发了病毒脂质膜与宿主细胞膜的融合。

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