Ifediba T C, Stern A, Ibrahim A, Rieder R F
Blood. 1985 Feb;65(2):452-5.
Studies of the ability of Plasmodium falciparum to grow in vitro in the red blood cells of subjects with certain beta-thalassemia syndromes are often difficult to interpret because of the known inhibitory effect of an elevated cellular content of human fetal hemoglobin (HbF). P falciparum therefore was cultured in vitro in the erythrocytes of subjects with hemoglobin H (HbH) disease and various other alpha-thalassemia genotypes that are unaccompanied by increased levels of HbF. Growth of the malaria parasite was markedly retarded in HbH red blood cells, when compared with growth in blood from normal control subjects. No consistent impairment of growth was seen in the erythrocytes of subjects having deletion of only one or two alpha-globin genes. These results indicate that erythrocytes with a severe thalassemia phenotype provide a less hospitable growth environment for P falciparum than normally hemoglobinized red blood cells, even in the absence of increased levels of HbF.
由于已知人类胎儿血红蛋白(HbF)细胞含量升高具有抑制作用,因此对恶性疟原虫在某些β地中海贫血综合征患者红细胞中体外生长能力的研究往往难以解释。因此,将恶性疟原虫在血红蛋白H(HbH)病患者以及其他各种未伴有HbF水平升高的α地中海贫血基因型患者的红细胞中进行体外培养。与正常对照受试者血液中的生长情况相比,疟原虫在HbH红细胞中的生长明显受阻。在仅缺失一个或两个α珠蛋白基因的受试者的红细胞中,未观察到一致的生长受损情况。这些结果表明,即使在没有HbF水平升高的情况下,具有严重地中海贫血表型的红细胞为恶性疟原虫提供的生长环境比正常血红蛋白化的红细胞更不适宜。