Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that the Duffy blood group negative genotype is a factor in resistance to Plasmodium vivax, we determined the Duffy blood group, the malaria antibodies, and the slide-demonstrated infection rates with P. vivax and P. falciparum of 420 persons living in Nueva Armenia, Honduras. In all, 247 persons were Duffy negative. Demonstrated infections with P. falciparum were almost equally distributed between Duffy-positive (5,8%) and Duffy-negative (4.9%) persons. Similarly, Duffy-positive (25.6%) and Duffy-negative (28.2%) persons had equal proportions of indirect fluorescent antibody test titers suggestive of past or present P. falciparum infection. In contrast, all 14 P. vivax infections were found in Duffy-negative persons. There was no evidence suggesting that Duffy-positive and Duffy-negative persons had different exposures to malaria. The Duffy negative genotype FyFy appears to be a factor in resistance to P. vivax.
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PMID:The Duffy blood group and resistance to Plasmodium vivax in Honduras. 35 34

The frequencies of the following blood group antigens: A, B, O, M, N, S, s, U, Fya, FyB, Lea, Jsa and K have been determined in Nigerian children with severe falciparum malaria. The frequency distribution of M, N, S, s, U, Fya and Fyb were not significantly different in children with life-threatening falciparum malaria and controls. The frequencies of A, B, O, Lea, Jsa and K found in the children with severe malaria were similar to those previously reported for healthy adults in this population. The Duffy blood group antigens Fya and Fyb were virtually absent from both infected and control children. This finding is in variance with a Fya frequency of 23% reported by Worlledge et al. (1974) for healthy adults in this population.
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PMID:Frequency of blood group antigens in Nigerian children with falciparum malaria. 38 66

Duffy blood group negative human erythrocytes (FyFy) are resistant to infection by Plasmodium knowlesi, a simian malaria that infects Duffy positive human erythrocytes. The P. knowlesi resistance factor, Duffy negative erythrocytes, occurs in high frequency in West Africa, where the people are resistant to vivax malaria. This suggests that Duffy blood group determinants (Fya or Fyb) may be erythrocyte receptors for P. vivax.
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PMID:Erythrocyte receptors for (Plasmodium knowlesi) malaria: Duffy blood group determinants. 114 13

Among a small group of Saudi Arabs the Duffy blood group (Fy(a-b-)) was found to be associated with the sickle cell trait more often than could be explained by random gene combination thus supporting the concept that African gene flow brought the sickle cell trait to the Arabian peninsula. Based on recent observations concerning the possible role of Fy(a-b-) as a resistance factor against vivax malaria, it is proposed that the gene combination AS FyFy is likely to be selected in areas where falciparum and vivax infections are endemic and mixed infections occur frequently.
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PMID:Association of Duffy blood groups with the sickle cell trait. 126 23

Blood samples from 324 malarial patients and 384 healthy individuals belonging to the Ao tribal community have been examined for Duffy blood group systems. The complete absence of Duffy-negative individuals among the Ao Nagas suggests that selection for resistance to vivax malaria by means of the Duffy-negative phenotype has not been available in the southeast Asian regions including the Ao Nagas.
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PMID:Duffy blood groups and malaria in the Ao Nagas in Nagaland, India. 178 11

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

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

Plasmodium vivax and the related monkey malaria, P. knowlesi, require interaction with the Duffy blood group antigen, a receptor for a family of chemokines that includes interleukin 8, to invade human erythrocytes. One P. vivax and three P. knowlesi proteins that serve as erythrocyte binding ligands in such interactions share sequence homology. Expression of different regions of the P. vivax protein in COS7 cells identified a cysteine-rich domain that bound Duffy blood group-positive but not Duffy blood group-negative human erythrocytes. The homologous domain of the P. knowlesi proteins also bound erythrocytes, but had different specificities. The P. vivax and P. knowlesi binding domains lie in one of two regions of homology with the P. falciparum sialic acid binding protein, another erythrocyte binding ligand, indicating conservation of the domain for erythrocyte binding in evolutionarily distant malaria species. The binding domains of these malaria ligands represent potential vaccine candidates and targets for receptor-blockade therapy.
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PMID:Identification of the erythrocyte binding domains of Plasmodium vivax and Plasmodium knowlesi proteins involved in erythrocyte invasion. 804 29

Plasmodium malariae has not been reported from Suriname since 1979. In 1989 an increasing number of P. vivax infections among Bush-negroes returning from the eastern part of the interior was reported in Paramaribo. A microscopical re-examination of all malaria cases in the eastern part of the country failed to confirm any P. vivax infections, but instead P. malariae infections were diagnosed. A study followed to determine the Duffy blood group antigens of 4 Bush-negroes allegedly with a P. vivax infection in their medical history and of 28 and 32 unselected Bush-negroes and Amerindians respectively. Three of the 4 former Bush-negroes had the FyB antigen, while only 7% of the unselected Bush-negroes had this antigen. This low frequency of the genotype is incompatible with reports of high P. vivax prevalences in Bush-negro populations. The Amerindians tested showed a low proportion of Fy0 genotype, which is compatible with the frequent diagnosis of P. vivax among this ethnic group. Reports of P. vivax infections among Bush-negroes are due to misdiagnosis of P. malariae, emphasizing the need to include all 4 species of human Plasmodium when (re)training microscopists. The question whether P. malariae reappeared in Suriname due to increased contact with the simian reservoir, or was simply missed, is discussed.
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PMID:Reappearance of Plasmodium malariae in Suriname? 823 78


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