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Glucose-6-phosphate dehydrogenase (G6PD; EC 1.1.1.49)-deficient red blood cells from male hemizygotes and female heterozygotes from the island of Sardinia were studied for their ability to support growth in vitro of the malaria-causing organism Plasmodium falciparum. Parasite growth was approximately one-third of normal in both hemi- and heterozygotes for G6PD deficiency. In Sardinians with the beta 0-thalassemia trait, parasite growth was normal except when G6PD deficiency occurred together with the thalassemia trait. The data support the hypothesis that G6PD deficiency may confer a selective advantage in a malarious area; the female heterozygote may be at a particular advantage because resistance to malaria equals that of male hemizygotes, but the risk of fatal hemolysis may be less. However, more female heterozygotes must be studied to confirm this hypothesis. No protective effect of beta 0-thalassemia trait could be demonstrated in vitro.
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
May 1987,
Blood,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
May 1965,
The American journal of tropical medicine and hygiene,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
April 2006,
The FEBS journal,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
June 1990,
Molecular and biochemical parasitology,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
October 1988,
Molecular and biochemical parasitology,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
April 1994,
Molecular and biochemical parasitology,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
October 2015,
The FEBS journal,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
June 2011,
The Biochemical journal,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
July 2012,
IUBMB life,
E F Roth, and
C Raventos-Suarez, and
A Rinaldi, and
R L Nagel
January 2021,
PloS one,
