1985
DOI: 10.1038/313793a0
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Adaptation of Plasmodium falciparum to glucose 6-phosphate dehydrogenase-deficient host red cells by production of parasite-encoded enzyme

Abstract: There is impressive evidence from geographical data, studies in the field and in vitro culture work that genetically determined deficiency of glucose 6-phosphate dehydrogenase (G6PD) confers relative protection against the human malaria parasite, Plasmodium falciparum. G6PD is encoded by an X-chromosome-linked gene, and protection phenomenon is manifested in heterozygous females who are genetic mosaics but, surprisingly, not in hemizygous males with complete deficiency. We have shown previously that the parasi… Show more

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Cited by 91 publications
(50 citation statements)
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“…Based on the aforementioned observations, it is reasonable therefore, to adduce that malaria parasites could grow better in the RBCs of G6PD non-deficient individuals than in the RBCs of the G6PD deficient ones, which could result to the high parasite density observed in nondeficient subjects. Our result, therefore, favours the malaria / G6PD deficiency hypothesis, which affirmed that G6PD deficiency, are contributing factors to malarial resistance (Usanga & Luzzatto, 1985). The result is also supported by the observation that more cohort G6PD non-deficient subjects, particularly children below 5 years of age were admitted in the hospital for the treatment of severe malaria than cohort G6PD deficient subjects during which severe malaria associated with symptoms including cerebral malaria, seizure, severe headache, vomiting, diarrhoea and respiratory distress, were evident.…”
Section: Discussionsupporting
confidence: 82%
“…Based on the aforementioned observations, it is reasonable therefore, to adduce that malaria parasites could grow better in the RBCs of G6PD non-deficient individuals than in the RBCs of the G6PD deficient ones, which could result to the high parasite density observed in nondeficient subjects. Our result, therefore, favours the malaria / G6PD deficiency hypothesis, which affirmed that G6PD deficiency, are contributing factors to malarial resistance (Usanga & Luzzatto, 1985). The result is also supported by the observation that more cohort G6PD non-deficient subjects, particularly children below 5 years of age were admitted in the hospital for the treatment of severe malaria than cohort G6PD deficient subjects during which severe malaria associated with symptoms including cerebral malaria, seizure, severe headache, vomiting, diarrhoea and respiratory distress, were evident.…”
Section: Discussionsupporting
confidence: 82%
“…This deficiency offers a selective protection against P.falciparum malaria (Roth et al, 1983). It has, however, been reported that some P.falciparum parasite strains have been able to synthesize their own G6PD enzyme thereby evading the immunity offered by G6PD deficiency in such individuals (Usanga and Luzzatto 1985). G6PD deficiency is also known to be associated with decreased phagocytic and bactericidal activity of phagocytes (Owusu 1978, Luzzatto 1975.…”
Section: Discussionmentioning
confidence: 99%
“…The relative protection of G-6-PD deficiency against P. falciparum postulated by Motulsky (1960) is manifested by the heterozygous females but not by the males who are hemizygous for the deficient gene (Bienzle et al 1972, Usanga & Luzzato 1985. Therefore, the absence of association between G-6-PD among males and the phenotypes involved in Plasmodium infection seen in Table I, as well as the significant association of the females symptomless for P. vivax with homozygosis for the gene Gd B has no practical meaning.…”
Section: Discussionmentioning
confidence: 99%