Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, National University Health System, Singapore; Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand.
Biomedicine Discovery Institute and Department of Microbiology, Monash University, Melbourne, Australia.
Trends Parasitol. 2017 Apr;33(4):321-334. doi: 10.1016/j.pt.2016.11.009. Epub 2016 Dec 29.
Our current understanding of how malaria parasites remodel their host red blood cells (RBCs) and ultimately cause disease is largely based on studies of Plasmodium falciparum. In this review, we expand our knowledge to include what is currently known about pathophysiological changes to RBCs that are infected by non-falciparum malaria parasites. We highlight the potential folly of making generalizations about the rheology of malaria infection, and emphasize the need for more systematic studies into the erythrocytic biology of non-falciparum malaria parasites. We propose that a better understanding of the mechanisms that underlie the changes to RBCs induced by malaria parasites other than P. falciparum may be highly informative for the development of therapeutics that specifically disrupt the altered rheological profile of RBCs infected with either sexual- or asexual-stage parasites, resulting in drugs that block transmission, reduce disease severity, and help delay the onset of resistance to current and future anti-malaria drugs.
我们目前对疟原虫重塑宿主红细胞(RBC)并最终导致疾病的理解在很大程度上基于对恶性疟原虫的研究。在这篇综述中,我们将知识扩展到包括目前已知的被非恶性疟原虫感染的 RBC 的病理生理变化。我们强调了对疟疾感染流变学做出泛泛之论的潜在愚蠢,并强调需要对非恶性疟原虫的红细胞生物学进行更系统的研究。我们提出,更好地了解除恶性疟原虫以外的疟原虫引起的 RBC 变化的机制,可能对开发专门破坏受感染 RBC 的改变的流变学特性的疗法具有高度的信息性,从而产生阻断传播、降低疾病严重程度和有助于延迟对当前和未来抗疟药物的耐药性的药物。