School of Medicine, Deakin University, Waurn Ponds, Victoria, Australia.
Cell Microbiol. 2019 Apr;21(4):e13009. doi: 10.1111/cmi.13009. Epub 2019 Feb 12.
Plasmodium parasites that cause the disease malaria have developed an elaborate trafficking pathway to facilitate the export of hundreds of effector proteins into their host cell, the erythrocyte. In this review, we outline how certain effector proteins contribute to parasite survival, virulence, and immune evasion. We also highlight how parasite proteins destined for export are recognised at the endoplasmic reticulum to facilitate entry into the export pathway and how the effector proteins are able to transverse the bounding parasitophorous vaculoar membrane via the Plasmodium translocon of exported proteins to gain access to the host cell. Some of the gaps in our understanding of the export pathway are also presented. Finally, we examine the degree of conservation of some of the key components of the Plasmodium export pathway in closely related apicomplexan parasites, which may provide insight into how the diverse apicomplexan parasites have adapted to survival pressures encountered within their respective host cells.
疟原虫寄生虫导致疟疾疾病已经开发出一种精细的运输途径,以促进数百种效应蛋白进入其宿主细胞——红细胞。在这篇综述中,我们概述了某些效应蛋白如何有助于寄生虫的存活、毒力和免疫逃避。我们还强调了如何在内质网识别即将出口的寄生虫蛋白,以促进进入出口途径,以及效应蛋白如何通过疟原虫输出蛋白的转运体跨越边界的寄生泡膜,从而进入宿主细胞。我们还提出了对出口途径理解中的一些空白。最后,我们研究了在密切相关的顶复门寄生虫中,一些关键的疟原虫输出途径的组成部分的保守程度,这可能有助于了解不同的顶复门寄生虫是如何适应其各自宿主细胞中遇到的生存压力的。