A case-control study in northern Liberia of<i>Plasmodium falciparum</i>malaria in haemoglobin S and β-thalassaemia traits

Willcox, M.; Björkman, Anders; Brohult, Johan; Po, Pehrson; Rombo, Lars; Bengtsson, Elias

doi:10.1080/00034983.1983.11811704

Cited by 84 publications

(43 citation statements)

References 14 publications

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“…Therefore, the people with sickle cell trait are more likely to reach reproductive age and pass their genes on to the next generation [2]. Willcox et al also reported similar conclusion in their studies [3].…”

Section: Malaria Defense and Sickle Cellsupporting

confidence: 72%

Sickle cell disease and malaria

Arif

2007

Indian J Hematol Blood Transfus

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Malaria is most common infectious disease spread by female Anopheles mosquitoes especially in tropical and subtropical areas of the world. It is reported by WHO as a 4th leading cause of death in children across the developing countries. Unfortunately no vaccine is currently available. Sickle cell trait (HbAS) patients provide some resistance for malaria over normal persons (HbAA) or their homozygous state (HbSS) due to various reasons.

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Section: Malaria Defense and Sickle Cellsupporting

confidence: 72%

Sickle cell disease and malaria

Arif

2007

Indian J Hematol Blood Transfus

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“…A first advantage is reduction in parasite growth and parasite density, observed in patients with HbAS and beta-thal trait 46,47 but not in patients with alpha-thal trait. Secondly, phagocytosed ring forms are digested rapidly by monocytes, and the process is repeated without loss of efficiency.…”

Section: Discussionmentioning

confidence: 99%

Enhanced phagocytosis of ring-parasitized mutant erythrocytes: a common mechanism that may explain protection against falciparum malaria in sickle trait and beta-thalassemia trait

Ayi

Turrini

Piga

et al. 2004

Blood

309

266

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High frequency of erythrocyte (red blood cell [RBC]) genetic disorders such as sickle cell trait, thalassemia trait, homozygous hemoglobin C (Hb-C), and glucose-6-phosphate dehydrogenase (G6PD) deficiency in regions with high incidence of Plasmodium falciparum malaria and casecontrol studies support the protective role of those conditions. Protection has been attributed to defective parasite growth or to enhanced removal of the parasitized RBCs. We suggested enhanced phagocytosis of rings, the early intraerythrocytic form of the parasite, as an alternative explanation for protection in G6PD deficiency. We show here that P falciparum developed similarly in normal RBCs and in sickle trait, beta-and alpha-thalassemia trait, and HbH RBCs. We also show that membrane-bound hemichromes, autologous immunoglobulin G (IgG) and complement IntroductionHigh frequency of hemoglobinopathies such as sickle cell trait, thalassemia trait, homozygous hemoglobin C (Hb-C) and Hb-E; glucose-6-phosphate dehydrogenase (G6PD) deficiency; and Southeast Asian ovalocytosis (SAO) in regions with past or present high incidence of Plasmodium falciparum malaria and case-control studies support the protective role of those conditions (see Roberts et al 1 ; Weatherall 2 ; Greene 3 ; and Serjeantson et al 4 for reviews). Protection has been attributed in some studies to defective invasion or growth of the parasite in the mutant erythrocytes (red blood cells [RBCs]), 5-7 while other studies found normal parasite invasion and growth. 8,9 Since the original proposal by Haldane, 10 microcitemia and increased osmotic resistance, enhanced oxidant radical production due to unpaired globin chains, increased sickling, ionic unbalances or membrane rigidity, or molecular defects in band 3 have been suggested as underlying mechanisms explaining impaired growth of the parasite in the mutant RBCs. [1][2][3][4][5][11][12][13] Other studies have found increased deposition of nonspecific autologous antibodies on malaria-parasitized mutant RBCs and suggested phagocytic elimination as the possible mechanism of protection in nonimmune subjects. 14-16 Recently, we found that several strains of P falciparum developed similarly in normal and G6PD-deficient RBCs. 9 However, ring-parasitized G6PD-deficient RBCs bound more opsonins such as autologous immunoglobulin G (IgG) and complement C3c fragments, and were phagocytosed more intensely than their normal counterparts. 9 We suggested enhanced ring phagocytosis as an alternative explanation for malaria protection in G6PD-deficient individuals, and discussed why removal of early parasite forms could be advantageous to the host. 9 We show here that P falciparum invaded and matured similarly in normal and mutant RBCs (heterozygous sickle cell anemia [HbAS]; heterozygous beta-thalassemia [beta-thal trait]; homozygotes for alpha-plus thalassemia [alpha-thal trait]; compound heterozygotes for alpha-zero and alpha-plus thalassemia [HbH disease]) up to the third cycle of invasion. We also show that membrane-bound hemichromes, ag...

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“…Many of the reasons for this wide variation in the presentation of this disease have been known for years, such as the protection afforded by some hemoglobinopathies. 1,2 Recent scientific advancements and closer coordination of work done in various disciplines have begun to explain other observations for which there previously has been no satisfying explanation. For instance, application of newer genetic techniques to large populations has linked a particular human leukocyte antigen (HLA) type to increased risk of cerebral malaria, 3 partly explaining the observation that there are some people who develop cerebral malaria while most of their neighbors, with presumably the same exposures and histories, do not.…”

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confidence: 99%

Longitudinal cohort study of the epidemiology of malaria infections in an area of intense malaria transmission I. Description of study site, general methodology, and study population.

Bloland

Ruebush²,

McCormick³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

101

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Abstract. A large-scale longitudinal cohort project was initiated in western Kenya in June 1992. The primary purpose of the project was to study Plasmodium falciparum malaria in a highly endemic area using a comprehensive and multidisciplinary approach, which included epidemiology, entomology, and immunology. Between June 1992 and July 1994, pregnant women living in 15 rural villages were identified during a monthly census and 1,164 were enrolled. The women were followed-up throughout their pregnancy and they, along with their newborn infants and direct siblings of the infants' less than 15 years of age, were monitored over time. As of May 1995, 1,017 infants had been born to these women. This paper presents the design and general methodology used in this study and describes the initial experience with intense monitoring of a large population over a prolonged period.Plasmodium falciparum infection can present with a wide spectrum of signs, symptoms, and history, from a fatal disease to an apparently asymptomatic infection, from a rapidly progressing, fulminant illness to a chronic insult. Many of the reasons for this wide variation in the presentation of this disease have been known for years, such as the protection afforded by some hemoglobinopathies.1,2 Recent scientific advancements and closer coordination of work done in various disciplines have begun to explain other observations for which there previously has been no satisfying explanation. For instance, application of newer genetic techniques to large populations has linked a particular human leukocyte antigen (HLA) type to increased risk of cerebral malaria, 3 partly explaining the observation that there are some people who develop cerebral malaria while most of their neighbors, with presumably the same exposures and histories, do not. 4 Combining the work of entomologists with that of clinical epidemiologists has demonstrated an effect of exposure pressure on disease development. 5 Because of the growing realization of complex interrelationships among the parasite, vector, environment, and host, advancing our understanding of falciparum malaria will require investigation of most if not all of these factors simultaneously. Conducting studies with similar designs in a variety of epidemiologic settings may also be necessary to understand the determinants of the full range of malarial illness. While a tremendous amount has been and can still be learned from cross-sectional studies, many of the questions that remain can only be addressed by monitoring larger numbers of people over longer periods of time, such as has been done in Senegal, 6 Ghana, 7 and Nigeria. 8A study initiated in June 1992 in western Kenya was designed to address the epidemiology, entomology, immunology (both humoral and cellular responses to defined antigens), host factors, molecular biology and antigenic variation, and population genetics of P. falciparum in a large cohort of women, newborn infants, and older children monitored over an extended period. Taken as a whole, this project wil...

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A case-control study in northern Liberia ofPlasmodium falciparummalaria in haemoglobin S and β-thalassaemia traits

Cited by 84 publications

References 14 publications

Sickle cell disease and malaria

Sickle cell disease and malaria

Enhanced phagocytosis of ring-parasitized mutant erythrocytes: a common mechanism that may explain protection against falciparum malaria in sickle trait and beta-thalassemia trait

Longitudinal cohort study of the epidemiology of malaria infections in an area of intense malaria transmission I. Description of study site, general methodology, and study population.

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