scholarly journals Hemoglobin E and Glucose-6-Phosphate Dehydrogenase Deficiency and Plasmodium falciparum Malaria in the Chittagong Hill Districts of Bangladesh

2015 ◽  
Vol 93 (2) ◽  
pp. 281-286 ◽  
Author(s):  
Kerry L. Shannon ◽  
Myaing M. Nyunt ◽  
Sabeena Ahmed ◽  
Jasmin Akter ◽  
Ashish Chowdhury ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Falciparum Malaria ◽  
Dehydrogenase Deficiency ◽  
Plasmodium Falciparum Malaria ◽  
Hemoglobin E ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Infection with Plasmodium falciparum malaria in a patient with homozygous hemoglobin E

2019 ◽  
Vol 10 (1) ◽  
pp. 36
Author(s):  
Siris Patel ◽  
Prasanta Purohit ◽  
PradeepKumar Mohanty ◽  
Jogeswar Panigrahi
Keyword(s):  
Plasmodium Falciparum ◽  
Falciparum Malaria ◽  
Plasmodium Falciparum Malaria ◽  
Hemoglobin E ◽  
Homozygous Hemoglobin E

scholarly journals The effect of X chromosome inactivation on the inhibition of Plasmodium falciparum malaria growth by glucose-6-phosphate-dehydrogenase- deficient red cells

Blood ◽  
1983 ◽  
Vol 62 (4) ◽  
pp. 866-868 ◽  
Author(s):  
EF Jr Roth ◽  
C Raventos Suarez ◽  
A Rinaldi ◽  
RL Nagel
Keyword(s):  
Plasmodium Falciparum ◽  
Falciparum Malaria ◽  
Plasmodium Falciparum Malaria ◽  
Parasite Growth ◽  
Red Cells ◽  
Normal Cells ◽  
Hemizygous Male ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Cell Glucose

Abstract Previous data on in vitro culture of Plasmodium falciparum malaria demonstrated that red cell glucose-6-phosphate dehydrogenase deficiency (G6PD-) inhibited parasite growth in deficient hemizygous males. This study investigated the effect of heterozygosity for G6PD- on parasite growth. Blood was obtained from 8 female Sardinian G6PD- heterozygotes with G6PD normal cells ranging from 13% to 60%. For comparison, blood from a G6PD- hemizygous male, containing 100% deficient red cells, was mixed in different proportions with compatible normal blood. In both experiments, parasite growth was inhibited by the presence of deficient cells. In both cases, it was found that the inhibition could be explained by a simple dilution of normal cells by G6PD- cells. Thus, the typical female heterozygote is also protected to a significant extent. When considering the “malaria hypothesis” as it relates to G6PD, protection of the female heterozygote as well as the male hemizygote must be taken into account.

scholarly journals An overview on significant human genetics modification in the protection against severe Falciparum malaria

2018 ◽  
Vol 11 (1) ◽  
pp. 165-167
Author(s):  
Usman Ahmad
Keyword(s):  
Falciparum Malaria ◽  
Dehydrogenase Deficiency ◽  
Human Genetics ◽  
Genetically Modified ◽  
Beta Thalassemia ◽  
Hemoglobin F ◽  
Hemoglobin E ◽  
Hemoglobin C ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Severe Falciparum Malaria

This paper was aimed at expatiating the relevance to which falciparum malaria are protected due to various genetically modified factors which include Hemoglobin S, Hemoglobin E, Hemoglobin C, Hemoglobin F, Alpha and beta thalassemia, ovalocytosis, Glucose – 6- Phosphate dehydrogenase deficiency, Human leucocyte antigen (HLA) – BW53, DRBI 1302, DQBI 0501, Pyruvate kinase or PKLR gene. However, human genetics is one of the elements can be used in planning of co- ordinated attack on disease, since it sometime give an avenue to differentiate those groups or individual who are susceptible from those who are not.Keywords: malaria, hemoglobin, genetically modified factors

scholarly journals The effect of X chromosome inactivation on the inhibition of Plasmodium falciparum malaria growth by glucose-6-phosphate-dehydrogenase- deficient red cells

Blood ◽  
1983 ◽  
Vol 62 (4) ◽  
pp. 866-868
Author(s):  
EF Jr Roth ◽  
C Raventos Suarez ◽  
A Rinaldi ◽  
RL Nagel
Keyword(s):  
Plasmodium Falciparum ◽  
Falciparum Malaria ◽  
Plasmodium Falciparum Malaria ◽  
Parasite Growth ◽  
Red Cells ◽  
Normal Cells ◽  
Hemizygous Male ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Cell Glucose

Previous data on in vitro culture of Plasmodium falciparum malaria demonstrated that red cell glucose-6-phosphate dehydrogenase deficiency (G6PD-) inhibited parasite growth in deficient hemizygous males. This study investigated the effect of heterozygosity for G6PD- on parasite growth. Blood was obtained from 8 female Sardinian G6PD- heterozygotes with G6PD normal cells ranging from 13% to 60%. For comparison, blood from a G6PD- hemizygous male, containing 100% deficient red cells, was mixed in different proportions with compatible normal blood. In both experiments, parasite growth was inhibited by the presence of deficient cells. In both cases, it was found that the inhibition could be explained by a simple dilution of normal cells by G6PD- cells. Thus, the typical female heterozygote is also protected to a significant extent. When considering the “malaria hypothesis” as it relates to G6PD, protection of the female heterozygote as well as the male hemizygote must be taken into account.

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