Susceptibility to malaria

Nuchnoi P et al. (2008) Significant association between TIM1 promoter polymorphisms and protection against cerebral malaria in Thailand.

Allen SJ et al. (1999) Prevention of cerebral malaria in children in Papua New Guinea by southeast Asian ovalocytosis band 3.

Aitman TJ et al. (2000) Malaria susceptibility and CD36 mutation.

Patel SS et al. (2001) The association of the glycophorin C exon 3 deletion with ovalocytosis and malaria susceptibility in the Wosera, Papua New Guinea.

Fortin A et al. (2002) Susceptibility to malaria as a complex trait: big pressure from a tiny creature.

Hobbs MR et al. (2002) A new NOS2 promoter polymorphism associated with increased nitric oxide production and protection from severe malaria in Tanzanian and Kenyan children.

Maier AG et al. (2003) Plasmodium falciparum erythrocyte invasion through glycophorin C and selection for Gerbich negativity in human populations.

Omi K et al. (2003) CD36 polymorphism is associated with protection from cerebral malaria.

Rihet P et al. (2004) Hemoglobin C is associated with reduced Plasmodium falciparum parasitemia and low risk of mild malaria attack.

Fairhurst RM et al. (2005) Abnormal display of PfEMP-1 on erythrocytes carrying haemoglobin C may protect against malaria.

None (2005) How malaria has affected the human genome and what human genetics can teach us about malaria.

Campino S et al. (2006) Mendelian and complex genetics of susceptibility and resistance to parasitic infections.

Timmann C et al. (2007) Genome-wide linkage analysis of malaria infection intensity and mild disease.

Ayodo G et al. (2007) Combining evidence of natural selection with association analysis increases power to detect malaria-resistance variants.

Rowe JA et al. (2007) Blood group O protects against severe Plasmodium falciparum malaria through the mechanism of reduced rosetting.

Råberg L et al. (2007) Disentangling genetic variation for resistance and tolerance to infectious diseases in animals.

Moulds JM et al. (2000) Blood group associations with parasites, bacteria, and viruses.

Marquet S et al. (2008) A functional promoter variant in IL12B predisposes to cerebral malaria.

Auburn S et al. (2008) Association of the GNAS locus with severe malaria.

Sikora M et al. (2009) A variant in the gene FUT9 is associated with susceptibility to placental malaria infection.

Tripathi AK et al. (2009) Plasmodium falciparum-infected erythrocytes induce NF-kappaB regulated inflammatory pathways in human cerebral endothelium.

Louicharoen C et al. (2009) Positively selected G6PD-Mahidol mutation reduces Plasmodium vivax density in Southeast Asians.

Ferreira A et al. (2011) Sickle hemoglobin confers tolerance to Plasmodium infection.

Crosnier C et al. (2011) Basigin is a receptor essential for erythrocyte invasion by Plasmodium falciparum.

Timmann C et al. (2012) Genome-wide association study indicates two novel resistance loci for severe malaria.

Cserti-Gazdewich CM et al. (2012) Cytoadherence in paediatric malaria: ABO blood group, CD36, and ICAM1 expression and severe Plasmodium falciparum infection.

Turner L et al. (2013) Severe malaria is associated with parasite binding to endothelial protein C receptor.

Wanaguru M et al. (2013) RH5-Basigin interaction plays a major role in the host tropism of Plasmodium falciparum.

et al. (2014) Reappraisal of known malaria resistance loci in a large multicenter study.

Egan ES et al. (2015) Malaria. A forward genetic screen identifies erythrocyte CD55 as essential for Plasmodium falciparum invasion.

et al. (2015) A novel locus of resistance to severe malaria in a region of ancient balancing selection.

Kaushansky A et al. (2015) Malaria parasites target the hepatocyte receptor EphA2 for successful host infection.

Cappadoro M et al. (1998) Early phagocytosis of glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes parasitized by Plasmodium falciparum may explain malaria protection in G6PD deficiency.

Rowe JA et al. (1997) P. falciparum rosetting mediated by a parasite-variant erythrocyte membrane protein and complement-receptor 1.

Cockburn IA et al. (2004) A human complement receptor 1 polymorphism that reduces Plasmodium falciparum rosetting confers protection against severe malaria.

Tham WH et al. (2010) Complement receptor 1 is the host erythrocyte receptor for Plasmodium falciparum PfRh4 invasion ligand.

Schuldt K et al. (2010) FCGR2A functional genetic variant associated with susceptibility to severe malarial anaemia in Ghanaian children.

McGuire W et al. (1994) Variation in the TNF-alpha promoter region associated with susceptibility to cerebral malaria.

Knight JC et al. (1999) A polymorphism that affects OCT-1 binding to the TNF promoter region is associated with severe malaria.

Flori L et al. (2003) Linkage of mild malaria to the major histocompatibility complex in families living in Burkina Faso.

Clatworthy MR et al. (2007) Systemic lupus erythematosus-associated defects in the inhibitory receptor FcgammaRIIb reduce susceptibility to malaria.

Willcocks LC et al. (2010) A defunctioning polymorphism in FCGR2B is associated with protection against malaria but susceptibility to systemic lupus erythematosus.

Khor CC et al. (2007) A Mal functional variant is associated with protection against invasive pneumococcal disease, bacteremia, malaria and tuberculosis.

Martin SK et al. (1979) Severe malaria and glucose-6-phosphate-dehydrogenase deficiency: a reappraisal of the malaria/G-6-P.D. hypothesis.

Hill AV et al. (1992) Molecular analysis of the association of HLA-B53 and resistance to severe malaria.

Sjöberg K et al. (1992) Genetic regulation of human anti-malarial antibodies in twins.

Hill AV et al. (1991) Common west African HLA antigens are associated with protection from severe malaria.

Nagel RL et al. (1989) Malaria and red cell genetic defects.

Booth PB et al. (1972) The Gerbich blood group system, especially in Melanesians.

Bellamy R et al. () Absence of an association between intercellular adhesion molecule 1, complement receptor 1 and interleukin 1 receptor antagonist gene polymorphisms and severe malaria in a West African population.

Rihet P et al. (1998) Malaria in humans: Plasmodium falciparum blood infection levels are linked to chromosome 5q31-q33.

Kun JF et al. (1998) Polymorphism in promoter region of inducible nitric oxide synthase gene and protection against malaria.

Allen SJ et al. (1997) alpha+-Thalassemia protects children against disease caused by other infections as well as malaria.

Fernandez-Reyes D et al. (1997) A high frequency African coding polymorphism in the N-terminal domain of ICAM-1 predisposing to cerebral malaria in Kenya.

Williams TN et al. (1996) High incidence of malaria in alpha-thalassaemic children.

Serjeantson SW et al. (1994) A 3.5 kb deletion in the glycophorin C gene accounts for the Gerbich-negative blood group in Melanesians.

Ruwende C et al. (1995) Natural selection of hemi- and heterozygotes for G6PD deficiency in Africa by resistance to severe malaria.

Pasvol G et al. (1982) The interaction of malaria parasites with red blood cells.

Pasvol G et al. (1982) Erythrocytes deficiency in glycophorin resist invasion by the malarial parasite Plasmodium falciparum.

Kidson C et al. (1981) Ovalocytic erythrocytes from Melanesians are resistant to invasion by malaria parasites in culture.

Hadley T et al. (1983) Resistance of Melanesian elliptocytes (ovalocytes) to invasion by Plasmodium knowlesi and Plasmodium falciparum malaria parasites in vitro.

Roth EF et al. (1983) Glucose-6-phosphate dehydrogenase deficiency inhibits in vitro growth of Plasmodium falciparum.

Friedman MJ et al. (1981) The biochemistry of resistance to malaria.

None (1988) Elliptocytosis, malaria, and fertility in Malaysia.

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