The red cell cytoskeleton and invasion by malaria parasites

Facer, Christine A.

doi:10.1590/s0074-02761986000600018

Cited by 6 publications

(2 citation statements)

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“…(iii) Why have band 3 mutations in Papua New Guinea never occurred in Africa, and why has hemoglobin S never occurred in Papua New Guinea? Other erythrocyte skeletal mutations have been identified in Africa that appear to affect parasite development (5,6). (iv) Despite the slow evolution of the human genome compared to that of the parasite, the host innate resistance mechanisms can afford improved sur-vival.…”

Section: Estimates Of Mortality From Malariamentioning

confidence: 99%

Impact of malaria on genetic polymorphism and genetic diseases in Africans and African Americans.

Miller

1994

Proc. Natl. Acad. Sci. U.S.A.

108

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The high mortality from malaria in sub-Sahara Africa selected multiple genes that give the population a selective advantage. Identification of the genetic basis for resistance may suggest unusual approaches to development of malarial vaccines and antimalarial drugs. Some of these genes may be deleterious, although of selective advantage within the African setting, and need to be identified for counseling for disease prevention.

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Section: Estimates Of Mortality From Malariamentioning

confidence: 99%

Impact of malaria on genetic polymorphism and genetic diseases in Africans and African Americans.

Miller

1994

Proc. Natl. Acad. Sci. U.S.A.

108

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“…The increased rigidity of the erythrocyte membrane in SAO is thought to reduce the capacity of the band 3 proteins to cluster together, thereby making it more difficult for the malaria parasite to properly attaching to and enter the cell. The reduced free ATP within the cell has been postulated as a further mechanism behind which SAO creates a hostile environment for Plasmodium Falciparum [19][20][21][22][23][24][25].…”

Section: A Reduction In Expression Of Multiple Antigensmentioning

confidence: 99%

Man is not Sick by Germs alone-South East Asian Ovalocytosis, G6PD Deficiency, Erythrocyte Deformability and Experiments on Plasmodium Knowles Prove Germ Terrain Duality Theorem

Ayoade

2017

JOJNHC

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Erythrocytes carrying mutations in spectrin and protein 4.1 show differing sensitivities to invasion byPlasmodium falciparum

et al. 1995

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The role of the erythrocyte skeleton in the invasion process of Plasmodium falciparum was evaluated using genetically variant erythrocytes containing well-defined molecular defects in alpha spectrin (alpha Sp) or protein 4.1 from eight unrelated families. Invasion into red cells from subjects of three black families with hereditary pyropoikilocytosis (HPP) due to inheritance of alpha I/74 mutant spectrin was significantly reduced in cells both from the patients and from the relatives of these who carried asymptomatic hereditary elliptocytosis (HE). Likewise, reduced invasion was also seen in red cells from two families with HE in which the alpha I/65 variant spectrin was present. Resistance to invasion was not absolute in any sample and varied between 38% and 71% of that seen in normal cells. The decreased invasion correlated with the percentage of spectrin dimers present within the membrane of variant cells. In contrast, invasion into elliptocytes from three families that had a partial deficiency in protein 4.1 (HE/4.1+) but a normal percentage of spectrin dimers was either unchanged or increased. The precise mechanism and molecular basis behind the reduced invasion into HPP and HE red cells bearing Sp alpha I domain variants remains to be elucidated but might relate to alterations in merozoite/red cell-receptor interactions and/or merozoite endocytosis. The occurrence of elliptocytosis with spectrin defects (in particular, Sp alpha I/65 and Sp alpha I/46 variants in West Africa) suggests that these mutations of the alpha Sp gene could be related to some protection against malaria.

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The red cell cytoskeleton and invasion by malaria parasites

Cited by 6 publications

References 0 publications

Impact of malaria on genetic polymorphism and genetic diseases in Africans and African Americans.

Impact of malaria on genetic polymorphism and genetic diseases in Africans and African Americans.

Man is not Sick by Germs alone-South East Asian Ovalocytosis, G6PD Deficiency, Erythrocyte Deformability and Experiments on Plasmodium Knowles Prove Germ Terrain Duality Theorem

Erythrocytes carrying mutations in spectrin and protein 4.1 show differing sensitivities to invasion byPlasmodium falciparum

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