Sharp Paul M, Bibollet-Ruche Frederic, Hahn Beatrice H
Institute of Ecology and Evolution, University of Edinburgh, Edinburgh, UK.
Centre for Immunity, Infection and Evolution, University of Edinburgh, Edinburgh, UK.
Genome Biol Evol. 2025 Feb 3;17(2). doi: 10.1093/gbe/evaf016.
The human malaria parasite Plasmodium falciparum evolved from a parasite that infects gorillas, termed Plasmodium praefalciparum. The sialic acids on glycans on the surface of erythrocytes differ between humans and other apes. It has recently been shown that the P. falciparum cysteine-rich protective antigen (PfCyRPA) binds human sialoglycans as an essential step in the erythrocyte invasion pathway, while that of the chimpanzee parasite, Plasmodium reichenowi has affinities matching ape glycans. Two amino acid changes, at sites 154 and 209, were shown to be sufficient to switch glycan binding preferences and inferred to reflect adaptation of P. falciparum to humans. However, we show that sites 154 and 209 are identical in P. falciparum and P. praefalciparum, with no other differences located in or near the CyRPA glycan binding sites. Thus, the gorilla precursor appears to have already been preadapted to bind human sialoglycans.
人类疟疾寄生虫恶性疟原虫是从一种感染大猩猩的寄生虫——前恶性疟原虫进化而来的。人类和其他猿类红细胞表面聚糖上的唾液酸有所不同。最近有研究表明，恶性疟原虫富含半胱氨酸的保护性抗原（PfCyRPA）结合人类唾液酸聚糖是红细胞入侵途径中的关键步骤，而黑猩猩寄生虫——赖氏疟原虫的该抗原与猿类聚糖具有亲和力。研究显示，154位和209位的两个氨基酸变化足以改变聚糖结合偏好，并推测这反映了恶性疟原虫对人类的适应性。然而，我们发现恶性疟原虫和前恶性疟原虫的154位和209位氨基酸是相同的，在CyRPA聚糖结合位点或其附近没有其他差异。因此，大猩猩体内的原始寄生虫似乎已经预先适应了结合人类唾液酸聚糖。
