Coenzyme A synthesis in the human malaria parasite, Plasmodium falciparum

疟疾每年造成数亿病例，估计造成150万至270万人死亡。这种疾病是由一种微小的寄生虫引起的，这种寄生虫对抗疟疾药物的耐药性越来越强。很有可能在不久的将来，世界上某些地区的疟疾将成为一种无法治愈的疾病，因此迫切需要确定新的药物靶点。这项工作的重点是人类疟疾寄生虫恶性疟原虫的特定生化途径。该途径介导营养物质维生素B5转化为辅酶a分子，在红细胞内寄生虫中起重要作用，我们的初步数据表明，该途径的成分具有作为抗疟疾药物靶点的巨大潜力。在这个项目中，我们将使用一系列生化和分子生物学方法来详细描述寄生虫中这一途径的组成部分，并探索抑制这一途径的化合物可能作为急需的新型抗疟药的可能性。

Malaria is responsible for hundreds of millions of cases and an estimated 1.5-2.7 million deaths each year. The disease is caused by a microscopic parasite which is becoming increasingly resistant to antimalarial drugs. There is a very real possibility that there will soon be parts of the world in which malaria is an untreatable disease, and there is an urgent need to identify new drug targets. This work focuses on a particular biochemical pathway in the human malaria parasite, Plasmodium falciparum. The pathway mediates the conversion of the nutrient, vitamin B5, into a molecule called Coenzyme A. It plays an essential role in the intraerythrocytic parasite and our preliminary data indicate that components of this pathway hold significant potential as antimalarial drug targets. In this project we will use a range of biochemical and molecular biology approaches to characterise in detail the components of this pathway in the parasite and to explore the possibility that compounds that inhibit this pathway may be of value as much-needed new antimalarial agents.