I describe a model which posits the molecular basis of some malaria-resistance genes in the interaction between oxidized hemoglobin and membrane components The model is supported by a considerable body of evidence which indicates that erythrocytes of genetically protected individuals (carriers of sickle cell trait, α- and β-thalassemia, and G6PD deficiency) are susceptible to the increase of oxidation of hemoglobin following H2O2 release in the host cell by Plasmodium falciparum. I suggest that the irreversible interaction between oxidized hemoglobin and the red cell membrane could trigger mechanisms that: (i) reduce invasion of erythrocytes by the falciparum parasite, (ii) impair parasite survival and development within the cell, (iii) accelerate infected erythrocyte clearance by phagocytosis.
Genetic resistance to malaria, oxidative stress and hemoglobin oxidation / DESTRO-BISOL, Giovanni. - In: PARASSITOLOGIA. - ISSN 0048-2951. - STAMPA. - 41:1-3(1999), pp. 203-204.
Genetic resistance to malaria, oxidative stress and hemoglobin oxidation
DESTRO-BISOL, Giovanni
1999
Abstract
I describe a model which posits the molecular basis of some malaria-resistance genes in the interaction between oxidized hemoglobin and membrane components The model is supported by a considerable body of evidence which indicates that erythrocytes of genetically protected individuals (carriers of sickle cell trait, α- and β-thalassemia, and G6PD deficiency) are susceptible to the increase of oxidation of hemoglobin following H2O2 release in the host cell by Plasmodium falciparum. I suggest that the irreversible interaction between oxidized hemoglobin and the red cell membrane could trigger mechanisms that: (i) reduce invasion of erythrocytes by the falciparum parasite, (ii) impair parasite survival and development within the cell, (iii) accelerate infected erythrocyte clearance by phagocytosis.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.