Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Curr Opin Microbiol. 2013 Aug;16(4):445-51. doi: 10.1016/j.mib.2013.04.010. Epub 2013 May 29.
The continuous multiplication of Plasmodium parasites in red blood cells leads to a rapid increase in parasite numbers and is responsible for the disease symptoms of malaria. Survival and virulence of the parasite are linked to parasite-induced changes of the host red blood cells. These alterations require export of a large number of parasite proteins that are trafficked across multiple membranes to reach the host cell. Two classes of exported proteins are known, those with a conserved Plasmodium export element (PEXEL/HT) or those without this motif (PNEPs). Recent work has revealed new aspects of the determinants required for export of these 2 protein classes, shedding new light on the mode of trafficking during the different transport steps en route to the host cell.
疟原虫在红细胞中的持续繁殖导致寄生虫数量的快速增加,是疟疾症状的罪魁祸首。寄生虫的生存和毒力与寄生虫引起的宿主红细胞变化有关。这些改变需要大量的寄生虫蛋白输出,这些蛋白通过多种膜运输到达宿主细胞。已知有两类分泌蛋白,一类具有保守的疟原虫分泌元件(PEXEL/HT),另一类没有这种基序(PNEPs)。最近的工作揭示了这两类蛋白输出所需决定因素的新方面,为不同运输步骤中到达宿主细胞的运输方式提供了新的线索。