It is estimated that around one third of the global population are infected by弓形虫弓形虫。这种单细胞寄生虫会导致怀孕或免疫功能低下的人的严重疾病。感染是通过摄入粪便污染的土壤（在未洗净的水果和蔬菜上）或未煮过的肉食的寄生虫囊肿而发生的。Toxoplasma贡迪可以归类为我们所知道的最成功的寄生虫感染之一。它几乎可以感染所有温血动物和细胞类型。
此外，它甚至能够改变小啮齿动物的行为，使它们被猫掠食者所吸引。然后，啮齿动物被食用，寄生虫被传递给其确定的宿主：猫。这是寄生虫的非常成功的策略。
许多研究人员对Toxoplasmafor a different reason though: it can be used as a model organism to represent the biology of a similar parasite, namely the malaria parasite疟原虫。Toxoplasmaand疟原虫are both members of the apicomplexan phylum and possess similar cell structure and lifecycle features. However,Toxoplasma在实验室中比文化更容易恶性疟原虫orP. vivax,是一种较大的生物体，在遗传上更具遗传性，其生物安全水平较低。由于这些原因，许多工作要理解疟原虫invasion has focused around the wayToxoplasmamoves and invades cells. This is because they are both thought to share common gliding motility machinery.
滑行运动
滑行运动（（a type of movement whereby the cell moves along a surface without changing its shape) is unique to members of the Apicomplexa. This is in contrast to the common models of eukaryote cell movement where either a leading edge of the cell reaches forward, anchors, and the rear end follows (termed cell crawling) or motility is flagellar driven.
滑行运动可以使Apicomplexan寄生虫定位并进入宿主细胞。当他们不再支持寄生虫负载时，它还使他们可以离开宿主单元。为了Toxoplasma这发生在其裂解生命周期期间，是寄生虫在宿主组织中迅速传播的方式。疟原虫孢子虫还使用这种运动从细胞真皮传播到蚊子后的血管。
了解寄生虫完成其生命周期至关重要的个体机制对于检测药物和疫苗靶向候选物很重要。因此，许多小组一直在研究寄生虫滑行机械，目的是阻止寄生虫进入宿主细胞，从而使免疫系统消除了感染。
滑行运动involves actin and myosin working together in a system called the
肌动蛋白运动复合物。经常在参考人类肌肉细胞收缩的方式中描述Acto肌球蛋白系统，有几种显示此系统的YouTube视频。但是，在Toxoplasma这个系统是substrate-dependent and allows the single-celled parasite to move in forward and circular motions. The acto-myosin system is made up of a complex of molecules and is thought to generate the force that causes the parasite to glide.
最近对滑行运动机械的见解
最近，由Markus Meissner教授领导的小组一直在系统地淘汰形成肌动蛋白肌球蛋白运动复合物的基因。该过程涉及从寄生虫基因组中切除特定基因，因此它们无法生成相应的蛋白质。尽管淘汰了，但大约25％的寄生虫仍可以滑动并入侵细胞。这项工作有助于确定当前对肌动蛋白功能功能的缺陷Toxoplasma。
然后，作者观察到，敲除寄生虫缺乏承受剪切流动的能力。他们解决了Toxoplasmaacto-myosin system, rather than acting simply as a motor, is required for attachment to a cell and acts as a force transducer. In this newly hypothesised model, the acto-myosin complex regulates and transmits the force, rather than being the generator of the force itself. This opens up the question of which mechanism is actually generating the force? One suggestion in the report was that it could be the backward flow of the parasites’ own membrane. This mechanism will therefore be the subject of future studies.
对Toxoplasmaand疟原虫研究
This is an exciting area of research because the movement ofToxoplasmaand疟原虫对于他们的生存至关重要。确实已经观察到类似的发现疟原虫学习，运动需要附加和分离机制的地方以及驱动力。靶向A的疫苗疟原虫运动蛋白（陷阱）是试用但是，功效很低。也许对滑行运动机制的新见解将成为对两者进行测试的不同抑制剂的平台Toxoplasmaand疟原虫疗法。
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