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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction between merozoites of the human pathogen, Plasmodium vivax, and the Duffy blood group glycoprotein on the surface of human erythrocytes is essential for the invasion of erythrocytes and the survival of the parasite. We have identified a P. vivax protein of 135 to 140 kDa which binds with receptor-like specificity to the human Duffy blood group glycoprotein. This interaction can be specifically inhibited by purified Duffy glycoprotein and by pretreating erythrocytes with a monoclonal antibody directed against a novel Duffy determinant. A protein with similar specificity for the Duffy glycoprotein from the phylogenetically related simian malaria, P. knowlesi, is shown to be immunologically related by the generation of cross-reactive antibodies. Despite their shared properties, these two Duffy associating proteins from P. vivax and P. knowlesi differ in some aspects of their interaction with the Duffy glycoprotein. The identification of these proteins will help elucidate the molecular mechanisms of erythrocyte invasion by Plasmodium.
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PMID:Plasmodium vivax interaction with the human Duffy blood group glycoprotein: identification of a parasite receptor-like protein. 268 May 68

A 135-kD parasite protein, a minor component of the Plasmodium knowlesi malaria radiolabeled proteins released into culture supernatant at the time of merozoite release and reinvasion, specifically bound to human erythrocytes that are invaded and carry a Duffy blood group determinant (Fya or Fyb), but did not bind to human erythrocytes that are not invaded and do not carry a Duffy determinant (FyFy). Specific anti-Duffy antibodies blocked the binding of the 135-kD protein to erythrocytes carrying that specific Duffy determinant. Purified 135-kD protein bound specifically to the 35-45-kD Duffy glycoprotein on a blot of electrophoretically separated membrane proteins from Fya and Fyb erythrocytes but not from FyFy erythrocytes. Binding of the 135-kD protein was consistently greater to Fyb than to Fya both on the blot and on intact erythrocytes. The 135-kD protein also bound to rhesus erythrocytes that are Fyb and are invaded, but not to rabbit or guinea pig erythrocytes that are Duffy-negative and are not invaded. Cleavage of the Duffy determinant by pretreating Fyb human erythrocytes with chymotrypsin greatly reduced both invasion and binding of the 135-kD protein, whereas pretreating Fyb erythrocytes with trypsin had little effect on the Duffy antigen, the 135-kD protein binding, or on invasion. However, instances of invasion of other enzyme-treated erythrocytes that are Duffy-negative and do not bind the 135-kD protein suggest that alternative pathways for invasion do exist.
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PMID:Receptor-like specificity of a Plasmodium knowlesi malarial protein that binds to Duffy antigen ligands on erythrocytes. 283 62

Adults claiming resistance to malaria were identified in the Sennar region of central Sudan, where P. falciparum is hyperendemic but seasonal in transmission. Indirect fluorescent antibody (IFA) titers of sera from these individuals were comparable to those of malaria patients with positive blood films, indicating equal exposure, while in vitro antiparasitic activity of their sera tended to be higher, indicating an effective immunological response to falciparum malaria. Hemoglobin S (Hb S) was significantly more prevalent in adults resistant to malaria. This trait offers protection at the erythrocyte level and it is also possible that it could enhance the ability of carrier adults to acquire protective immunity. Erythrocyte 6-phosphogluconate dehydrogenase A (PGDA) and phosphoglucomutase 1 (PGM1), phenotypes of unknown relevance to protection against falciparum malaria, were also significantly more prevalent in those claiming resistance to malaria. A trend of higher prevalence for erythrocyte glucose-6-phosphate dehydrogenase deficiency (G6PD-), Kell (+) and transferrin D (TfD) was detected among resistant individuals and higher KP(a+) and P2 among malaria patients, but the numbers evaluated in this study did not allow determination of statistical significance. No association was found with erythrocyte glyoxalases, ABO and Duffy blood groups and serum haptoglobins.
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PMID:Resistance to falciparum malaria among adults in central Sudan. 293 61

Plasmodium knowlesi, a malaria of Old World monkeys, invades all Duffy blood group positive human erythrocytes and various New World monkey erythrocytes except Cebus apella. We had previously identified a 135 kDa parasite protein in supernatants of P. knowlesi cultures that bound to Duffy positive but not to Duffy negative human erythrocytes [Haynes et al., J. Exp. Med. 167, 1873-1881 (1988)]. We now use New World monkey erythrocytes as a reagent to identify P. knowlesi proteins in culture supernatants that will bind to all New World monkey erythrocytes susceptible to invasion but not to C. apella erythrocytes, which are refractory to invasion. The 135 kDa protein binds to all New World monkey erythrocytes, including C. appella. Another protein of 155 kDa binds to all New World monkey erythrocytes except C. apella. The 155 kDa protein binds to Old World monkey erythrocytes, the natural host of P. knowlesi; it does not bind to human Duffy positive erythrocytes. This and the previous study are the beginning of the identification of parasite proteins of P. knowlesi that bind to erythrocytes in a receptor specific manner.
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PMID:Identification of Plasmodium knowlesi erythrocyte binding proteins. 322 9

189 healthy controls and 175 patients suffering from malaria vivax have been investigated with regard to associations between this disease and 22 genetic polymorphisms of the blood (ABO, MN, Ss, Rh, Kell, P, Lutheran, Kidd, Duffy, Diego, Xg; ABH-Secretor; Hp, Gc, Gm, Km; aP, AK, PGM1, 6-PGD, EsD; Hb variants) Significant associations could be demonstrated only for P and Hp systems, though in accordance with other investigations it cannot be excluded that the ABO system plays also a role in this connection.
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PMID:Genetic markers and malaria. Observations in Gujarat, India. 351 22

The A, B, O, D, Du, C, c, E, e, M, N, S, s, Kell and Duffy antigens were determined on 190 blood samples from Hausas in the north of Nigeria. The highest gene frequencies in the rhesus system were cDe (0.648) and cde (0.176). Su gene frequency was 0.270. The great majority of subjects were Kell negative (98.9%) and Duffy negative (98.8%). As the MNSs group determinants are carried by glycophorins, which are also receptor sites for Plasmodium falciparum, and the Duffy antigen marks the receptor for P. vivax, the present study provides data of interest in the epidemiology and genetics of malaria.
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PMID:Some red cell antigens in the Hausa population of northern Nigeria. 393 Mar 87

It is difficult to overestimate the evolutionary pressures exerted over the past few thousand years by endemic malaria. For most of hominid evolution, these parasites probably caused little morbidity and mortality. However, as Livingstone (1964, 1967, 1971) has pointed out, the advent of slash and burn horticulture and associated sedentary living patterns dramatically changed this situation. For many human populations, endemic malaria became an evolutionary emergency. In such pressing circumstances, genetic traits which ordinarily would carry with them an intolerable genetic load actually increase in frequency. Thus, although a few antimalarial red cell characteristics such as Duffy negativity are evidently innocuous, the majority of malaria-selected traits are not. Ovalocytosis, the abnormal hemoglobins and G-6-PD deficiencies are all quite deleterious in the homo- or hemizygote. This, more than anything else, bespeaks the extraordinary evolutionary pressures exerted by malaria. Needless to say, the mechanisms by which these various red cell traits protect are incompletely known. Although our discussion of such mechanisms has revolved about parasite/host cell relationships, the actual antimalarial effect may involve more distal interactions, especially of infected erythrocytes with the immune and reticuloendothelial systems. Protection exerted by modifications of such interactions would not be revealed by in vitro culture experiments upon which we rely for much of our information. For example, as normal red cells age and senesce, they express novel surface antigens which are recognized by specific immunoglobulins (Kay, 1983). Cells which have bound such antibodies are likely recognized and destroyed rapidly by the reticuloendothelial system. The expression of such senescence antigens may be hastened in already abnormal cells subject to the additional burden of an internal parasite. Therefore, it is quite possible that congenital defects of the red cell membrane, hemoglobin and metabolism may afford protection against malaria via immunologic mechanisms rather than by blocking penetration or predisposing the cell to spontaneous intravascular lysis. To be successful in the mammalian host, erythrocytic phase of malaria must recognize and attach to the host red cell, successfully penetrate, and replicate within. Remarkably, there are antimalarial red cells which impair each one of these individual steps. In this case, the ingenuity of natural selection has been almost--but not quite--a match for that of the malaria parasite.
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PMID:Antimalarial red cells. 639 Apr 55

Genetic markers have recently been found to be much more polymorphic than expected. Such extensive human polymorphisms may be partly explained by a number of genetic and environmental factors, including infectious diseases. Malaria, which was very widespread in the past and still poses a problem in many countries today, is a good candidate for research. The association between malaria and glucose-6-phosphate dehydrogenase (G6PD) deficiency is well-known, but more should be done to determine the mechanisms responsible for this positive correlation and to confirm that malaria is a strong selective factor for many other genotypes also. The present paper refers to a WHO project on genetic markers and susceptibility to infectious diseases, which is concerned mainly with G6PD deficiency and the following genetic markers: haemoglobinopathies, including the beta-thalassaemia trait and ABO, Rh, MN, Duffy, secretory types (Ss), and human leukocyte antigens (HLA). Since malaria was eradicated in Bulgaria many years ago, human populations from this country, living at different altitudes above sea-level, were used as a model for analysis of the malaria hypothesis. The data for G6PD deficiency confirm that malaria was a selective factor in lowland areas where malaria infection was more frequent in the past. It is, moreover, apparent that in addition to malaria some other factors also play a selective role.
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PMID:Frequency of glucose-6-phosphate dehydrogenase deficiency in relation to altitude: a malaria hypothesis. 696 37

We investigated an hypothesis relating the Duffy-negative blood type with insusceptibility to vivax malaria--and previously associated only with people of West African ancestry--in three population samples of eastern African stock. The samples included Nilotic and Hamitic-Semitic residents of a malarious locale in Ethiopia and Hamito-Semites in Addis Ababa where malaria is not endemic. Fresh red blood cells from 191 subjects were tested with Duffy antisera, anti-Fya and anti-Fyb. Duffy-positive rates in the malarious community were 8% for the Nilotes and 70% for the Hamito-Semites; the Hamito-Semites in Addis Ababa were 98% Duffy-positive. The relative prevalences of Plasmodium vivax in the two study groups at risk to malaria were 2.4% for the Nilotes and 27.3% for the Hamito-Semites, producing a ratio similar to the ratio of Duffy-positive in the two samples. We interpret the data as supportive of the Duffy-vivax hypothesis with reference to a part of eastern Africa, and we suggest that the Duffy-negative genotype may represent the original, rather than the mutant, condition in tropial Africa.
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PMID:Duffy blood types and vivax malaria in Ethiopia. 701 88

The people of Vanuatu exhibit several different genetic red cell polymorphisms. Some of these, such as alpha thalassaemia, are thought to have reached a high frequency as a result of selection pressure by malaria. In this study three rare blood group antigen variants, En(a-), Gerbich negative and Duffy negative, which are thought to confer a protective effect against malaria were sought in a sample of 214 (187 in the case of Duffy) from Espiritu Santo, Vanuatu. No individuals bearing these rare variants were found. The original settlers in Vanuatu are thought to have migrated from Papua New Guinea some 5,000 years ago, so it is of interest to note that no individuals were found to be Gerbich negative despite a high frequency in Melanesians living on some coastal parts of Papua New Guinea.
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PMID:A survey for the rare blood group antigen variants, En(a-), Gerbich negative and Duffy negative on Espiritu Santo, Vanuatu in the South Pacific. 755 53


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