MECHANISMS FOR HIV-1 ENHANCEMENT OF EICOSANOID FORMATION

HIV-1 增强类二十烷酸形成的机制

• 批准号: 3777544
• 负责人: T ELING
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3777544
• 关键词: arachidonate; clone cells; eicosanoids; human immunodeficiency virus 1; human tissue; monocyte; prostaglandins; virus envelope

The object of this project is to determine the mechanism by which the coat proteins (GP-120 and GP-160) from the AID virus enhances the formation of eicosanoids. Our initial effort was devoted to examining several cellular systems, human monocytes, Jurkat T cells and the monocyte line, THP-1 for their ability of metabolizing arachidonic acid to prostaglandins. Preliminary results indicate that the Jurkat cells form only minor amounts of prostaglandins and may not be a suitable model. We are in the process of testing a number of different preparations of GP-120 and GP-160 from several HIV strain for their ability to stimulate PGE2 from human monocytes. We are in the very early phase of this investigation.

本项目的目的是确定 来自AID病毒的外壳蛋白（GP-120和GP-160）增强了 类花生酸的形成。 我们最初的努力是研究 几种细胞系统，人单核细胞，Jurkat T细胞和 单核细胞系THP-1代谢花生四烯酸的能力， 兰丁 初步结果表明，Jurkat细胞 仅含有少量前列腺素，可能不是合适的模型。 我们正在测试一些不同的制剂， GP-120和GP-160的抗HIV活性 来自人单核细胞的PGE 2。 我们正处于这方面的早期阶段 调查