Impairment of the Growth of Plasmodium Falciparum in HbEE Erythrocytes

Nagel, Ronald L.; Raventós-Suárez, Carmen; Fabry, Mary E.; Tanowitz, Herbert B.; Sicard, Didier; Labie, Dominique

doi:10.1172/jci110248

Cited by 50 publications

(18 citation statements)

References 9 publications

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“…Various host cell conditions may affect some of these processes. [31][32][33][34][35][36][37] Evidence from the present study suggests that abnormal intraerythrocytic development affects parasite multiplication in CC cells. Parasites invaded AA and CC cells to a similar extent and we did not observe an accumulation of schizonts that would have indicated a block in merozoite release.…”

Section: Discussionmentioning

confidence: 99%

Aberrant development of Plasmodium falciparum in hemoglobin CC red cells: implications for the malaria protective effect of the homozygous state

Fairhurst

Fujioka

Hayton

et al. 2003

Blood

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Section: Discussionmentioning

confidence: 99%

Aberrant development of Plasmodium falciparum in hemoglobin CC red cells: implications for the malaria protective effect of the homozygous state

Fairhurst

Fujioka

Hayton

et al. 2003

Blood

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“…It is already established by in vitro analyses that p. falciparum grows slowly in homozygous HbE containing RBCs but not in the heterozygous one (Nagel et al 1981;Vemes et al 1986). It is shown to be due to the membrane abnormality which includes the differences in membrane rigidity particularly in glycophorin and sialic acid content (Chotivanish 2002).…”

Section: Hemoglobin E and Malariamentioning

confidence: 99%

Hemoglobin E in Northeast India: A review on its origin, distribution, migration and health implication

Sikdar

2016

Anthropological Review

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A systematic review of the studies on hemoglobin E in Northeast India has been carried out to understand the magnitude of research undertaken on this aspect during the last seven decades. Owing to the high prevalence of hemoglobin E in this part of India different authors have studied this hemoglobin from different perspectives and found conflicting results. However a systematic review of such studies is lacking from a holistic point of view. Most of the epidemiological, in vitro as well as in vivo studies show signatures of selection with this hemoglobin locus. However, how this polymorphism is maintained at different rates at different geographical region is still a matter of contention. This review will fill the gap from all perspectives starting from the frequency distribution of hemoglobin E and its spread in different parts of Northeast India, its relationship with malaria hypothesis, the population migration, population affinity and most importantly the health implication arising out of it. A probable origin of hemoglobin E among an Austroasiatic population of Northeast India has been postulated with the help of advance molecular anthropological knowledge like the deep rooted markers of mt DNA and Y-chromosome haplotypes.

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“…Hemoglobin E (HbE) is produced when the glutamic acid in position 26 of the β-globin chain is replaced by a lysine (Nagel et al, 1981;Chotivanich et al, 2002;Ohashi et al, 2004). It has been observed that erythrocytes from people having HbE show reduced plasticity and deformability "in vitro", thus impairing merozoite growth and release (Bunyaratvej et al, 1992).…”

Section: Hemoglobin E (Hbe)mentioning

confidence: 99%

“…It has been observed that erythrocytes from people having HbE show reduced plasticity and deformability "in vitro", thus impairing merozoite growth and release (Bunyaratvej et al, 1992). Homozygous HbE erythrocytes (HbEE) are microcytic (having low mean corpuscular volume) at low hemoglobin concentration (Nagel et al, 1981). Such hemoglobinopathy is very common in Southeastern Asia (Chotivanich et al, 2002) (Fig.…”

Section: Hemoglobin E (Hbe)mentioning

confidence: 99%