Snounou G, Jarra W, Preiser P R
Department of Infection and Tropical Medicine, Imperial College School of Medicine, Northwick Park Hospital, Harrow, Middlesex, UK.
Parasitol Today. 2000 Jan;16(1):28-30. doi: 10.1016/s0169-4758(99)01546-x.
In this article, Georges Snounou, William Jarra and Peter Preiser discuss the survival strategy of malaria parasites in the light of a novel mechanism of clonal phenotypic variation recently described for a multigene family of Plasmodium yoelii yoelii. The 235 kDa rhoptry proteins (Py235) encoded by these genes may be involved in the selection of red blood cells for invasion by merozoites. The new mechanism may explain the ability of individual parasites to adapt to natural variations in red blood cell subsets, while ensuring that sufficient merozoites escape immune attack, thus maintaining a chronic infection for extended periods. This counterpoints the antigenic variation exemplified by PfEMP1 proteins (a large family of proteins derived from P. falciparum), which operates at the population level. The possibility of manipulating the expression of functionally similar genes in other Plasmodium species could lead to therapies aimed at reducing clinical severity without compromising the acquisition and maintenance of immunity.
在本文中，乔治·斯诺努、威廉·贾拉和彼得·普雷泽根据最近描述的约氏疟原虫多基因家族的克隆表型变异新机制，讨论了疟原虫的生存策略。这些基因编码的235 kDa棒状体蛋白（Py235）可能参与裂殖子入侵红细胞的选择过程。这一新机制或许可以解释单个疟原虫适应红细胞亚群自然变异的能力，同时确保有足够的裂殖子逃脱免疫攻击，从而长期维持慢性感染。这与以PfEMP1蛋白（源自恶性疟原虫的一大类蛋白质）为例的抗原变异形成对比，后者在群体水平上发挥作用。在其他疟原虫物种中操纵功能相似基因表达的可能性，可能会带来旨在降低临床严重程度而又不影响免疫力获得和维持的治疗方法。
