Shear H L, Roth E F, Ng C, Nagel R L
Department of Medical and Molecular Parasitology, New York University School of Medicine, N.Y.
Br J Haematol. 1991 Aug;78(4):555-60. doi: 10.1111/j.1365-2141.1991.tb04488.x.
Inbred mice carrying mutations in ankyrin and/or spectrin synthesis and assembly were studied for their ability to support the growth of the rodent malarias, Plasmodium chabaudi adami and P. berghei, in vivo. Mice carrying the nb/nb (normoblastosis) mutation which do not synthesize ankyrin and therefore also have a deficiency in membrane-bound spectrin, were refractory to P. chabaudi adami, which invades mature erythrocytes and to P. berghei, which invades reticulocytes. Similarly, sph/sph mice which do not synthesize the alpha chain of spectrin but do synthesize ankyrin, were also resistant to both parasites. The heterozygote for the nb defect (nb/+) exhibited a diminution of parasitaemia. We conclude that the host cell spectrin may be necessary for the invasion and/or growth of rodent malarial parasites.
研究了携带锚蛋白和/或血影蛋白合成与组装突变的近交系小鼠在体内支持啮齿动物疟疾（查巴迪疟原虫和伯氏疟原虫）生长的能力。携带nb/nb（成红细胞增多症）突变的小鼠不合成锚蛋白，因此膜结合血影蛋白也缺乏，对侵入成熟红细胞的查巴迪疟原虫和侵入网织红细胞的伯氏疟原虫具有抗性。同样，不合成血影蛋白α链但合成锚蛋白的sph/sph小鼠对这两种寄生虫也具有抗性。nb缺陷的杂合子（nb/+）表现出寄生虫血症的减少。我们得出结论，宿主细胞血影蛋白可能是啮齿动物疟原虫入侵和/或生长所必需的。
