Aikawa M, Iseki M, Barnwell J W, Taylor D, Oo M M, Howard R J
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio.
Am J Trop Med Hyg. 1990 Aug;43(2 Pt 2):30-7. doi: 10.4269/ajtmh.1990.43.30.
Blockage of the cerebral microvasculature by Plasmodium falciparum-infected erythrocytes appears to be the principal cause of human cerebral malaria. Knobs which appear on the membrane of the infected erythrocytes adhere to the endothelium, causing the obstruction of cerebral microvessels. Protein molecules such as CD36, thrombospondin, and intercellular adhesion molecule-1, which are present on the membrane of endothelial cells, may act as receptors for the attachment of knobs of P. falciparum-infected erythrocytes. Each of these candidate host molecules for infected-cell recognition and attachment are expressed in microvessels of the human brain. The presence of HRP1 and HRP2 in the cerebral microvessels of cerebral malaria patients may indicate the involvement of knob proteins in the pathogenesis of cerebral malaria. Owl monkeys infected with P. falciparum do not develop cerebral malaria. There is no blockage of cerebral microvessels by infected erythrocytes and knob proteins are absent. These findings support the contention that cerebral microvessel blockage and the presence of knob proteins are the probable causes of cerebral malaria.
恶性疟原虫感染的红细胞对脑微血管的阻塞似乎是人类脑型疟疾的主要病因。出现在被感染红细胞膜上的隆起物会黏附在内皮上，导致脑微血管阻塞。存在于内皮细胞膜上的蛋白质分子，如CD36、血小板反应蛋白和细胞间黏附分子-1，可能作为恶性疟原虫感染红细胞隆起物附着的受体。这些用于识别和附着感染细胞的候选宿主分子中的每一种都在人类大脑的微血管中表达。脑型疟疾患者脑微血管中存在HRP1和HRP2，这可能表明隆起蛋白参与了脑型疟疾的发病机制。感染恶性疟原虫的夜猴不会患脑型疟疾。感染的红细胞不会阻塞脑微血管，且不存在隆起蛋白。这些发现支持了脑微血管阻塞和隆起蛋白的存在可能是脑型疟疾病因的观点。
