TY - JOUR
T1 - Malaria in β-thalassemic mice and the effects of the transgenic human β-globin gene and splenectomy
AU - Roth, Eugene F.
AU - Shear, Hannah L.
AU - Costantini, Frank
AU - Tanowitz, Herbert B.
AU - Nagel, Ronald L.
PY - 1988/1
Y1 - 1988/1
N2 - To investigate the protective effects of β-thalassemia against malaria, rodent malaria parasites were studied in C57BL/6J mice with β-thalassemia, in mice in which the thalassemia had been transgenically corrected with the human βA-globin gene, and in hematologically normal mice. In thalassemic mice, Plasmodium chabaudi adami infection was inhibited and peak parasitemia was variably delayed. In transgenically corrected mice, infection proceeded as in normal mice. Plasmodium berghei infection proceeded more rapidly in thalassemic mice, but survival was not different. Splenectomized normal mice displayed high-level parasitemia that peaked twice and persisted as a low-level parasitemia for more than 20 days after normal intact mice were free of all parasites. Splenectomized thalassemic mice showed a delay of 5 days in attaining peak parasitemia, but the parasitemia persisted as in normal splenectomized mice. Thus, for P. chabaudi, which displayed no preference for immature erythrocytes, β-thalassemia offers enhanced resistance for the host. However, for P. berghei, which preferentially invades reticulocytes, thalassemia is not protective. The protective effects of the normal mouse spleen were observed, but the paradoxical facilitation of parasite growth by the thalassemic spleen is a new finding that will require further experimentation to explain. This new in vivo laboratory documentation of thalassemic protection against some rodent malaria parasites may serve as a useful model in further efforts to control this major infectious disease.
AB - To investigate the protective effects of β-thalassemia against malaria, rodent malaria parasites were studied in C57BL/6J mice with β-thalassemia, in mice in which the thalassemia had been transgenically corrected with the human βA-globin gene, and in hematologically normal mice. In thalassemic mice, Plasmodium chabaudi adami infection was inhibited and peak parasitemia was variably delayed. In transgenically corrected mice, infection proceeded as in normal mice. Plasmodium berghei infection proceeded more rapidly in thalassemic mice, but survival was not different. Splenectomized normal mice displayed high-level parasitemia that peaked twice and persisted as a low-level parasitemia for more than 20 days after normal intact mice were free of all parasites. Splenectomized thalassemic mice showed a delay of 5 days in attaining peak parasitemia, but the parasitemia persisted as in normal splenectomized mice. Thus, for P. chabaudi, which displayed no preference for immature erythrocytes, β-thalassemia offers enhanced resistance for the host. However, for P. berghei, which preferentially invades reticulocytes, thalassemia is not protective. The protective effects of the normal mouse spleen were observed, but the paradoxical facilitation of parasite growth by the thalassemic spleen is a new finding that will require further experimentation to explain. This new in vivo laboratory documentation of thalassemic protection against some rodent malaria parasites may serve as a useful model in further efforts to control this major infectious disease.
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M3 - Article
C2 - 3335824
AN - SCOPUS:0023845116
SN - 0022-2143
VL - 111
SP - 35
EP - 41
JO - The Journal of Laboratory and Clinical Medicine
JF - The Journal of Laboratory and Clinical Medicine
IS - 1
ER -