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Suszeptibilität für Malaria

Malaria ist eine lebensbedrohlich Parasitenerkrankung, die durch Plasmodien hervorgerufen und durch die Anopheles Mücke übertragen wird. Die Ausprägung der Erkrankung wird durch verschiedene genetische Faktoren beeinflusst.

Gliederung

Erbliche Infektionsanfälligkeiten
Aspergillose-Infektionsanfälligkeit
Familiäre Candidose
HIV-Resistenz
IRAK4-Mangel
Invasive Pneumokokken-Erkrankung
Masern-Infektanfälligkeit
Meningokokken-Infektanfälligkeit
Resistenz gegenüber Trypanosoma brucei
Septischer Schock
Störungen der mRNA-Editiertfunktion
Suszeptibilität für Bakteriämie 1
Suszeptibilität für Malaria
FCGR2A
FCGR2B
TNF
Suszeptibilität für Mykobakteriosen
Suszeptibilität für Pseudomonas-Infektionen
X-chromosomale Suszeptibilität für Mykobakteriosen durch IKBKG-Defekt

Referenzen:

1.

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2.

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

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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.

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

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

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26.

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

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

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31.

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32.

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

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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.

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

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

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36.

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

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37.

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

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38.

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

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39.

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

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

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41.

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

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42.

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

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43.

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

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44.

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

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

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

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50.

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51.

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

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52.

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

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53.

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

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54.

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.

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55.

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

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56.

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

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57.

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58.

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59.

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60.

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61.

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62.

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

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63.

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

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64.

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

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65.

Orphanet article

Orphanet ID 673 external link
66.

OMIM.ORG article

Omim 611162 external link
67.

Wikipedia Artikel

Wikipedia DE (Malaria) external link
Update: 14. August 2020
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