Significantly upregulated expression of the DARC receptor in FyA/FyB heterozygote patients is suggestive of a greater receptor repertoire responsible for the possible variation in the parasite ligand binding with the host receptor and thus might have a role to play in severe malaria.
As it accumulates in plasma and urine during the blood stage of <i>Plasmodium</i> infection, labile heme is detoxified in RPTEC by HO-1 and FTH, preventing the development of acute kidney injury, a clinical hallmark of severe malaria.
For Plasmodium falciparum, the major cause of severe malaria in humans, a heterotrimeric complex comprised of the secreted parasite proteins, PfCyRPA, PfRIPR and PfRH5 is essential for erythrocyte invasion, mediated by the interaction between PfRH5 and erythrocyte receptor basigin (BSG).
Angiopoietin-1 (Ang-1) is a key regulator of angiogenesis and endothelial activation and has been studied as an objective biomarker in disease states such as atherosclerosis, sepsis, and severe malaria.
Integrated OMICS platforms identify LAIR1 genetic variants as novel predictors of cross-sectional and longitudinal susceptibility to severe malaria and all-cause mortality in Kenyan children.
For Plasmodium falciparum, the major cause of severe malaria in humans, a heterotrimeric complex comprised of the secreted parasite proteins, PfCyRPA, PfRIPR and PfRH5 is essential for erythrocyte invasion, mediated by the interaction between PfRH5 and erythrocyte receptor basigin (BSG).
Conversely, children with uncomplicated malaria showed a higher proportion of CD4<sup>+</sup> T cells expressing CD39 and Granzyme B, compared to children with complicated malaria.
Whereas the receptor-ligand association has revealed risk association against KIR2DS2-HLAC1 (OR=2.08, p-value=0.0229), KIR2DL3-HLAC1 (OR=1.79, p-value=0.0301), and KIR2DL1-HLAC2 (OR=2.10, p-value=0.0175) combinations for complicated malaria.
DUP4 is a complex structural genomic variant that carries extra copies of a glycophorin A-glycophorin B fusion gene and has a dramatic effect on malaria risk by reducing the risk of severe malaria by up to 40%.
Our data not only reinstates that CD14 of TLR pathway plays a predominant role in P. falciparum malaria, it establishes a functional basis for genetic association of rs5744454 with P. falciparum severe malaria by demonstrating a cis-regulatory role of this promoter polymorphism.
Whereas the receptor-ligand association has revealed risk association against KIR2DS2-HLAC1 (OR=2.08, p-value=0.0229), KIR2DL3-HLAC1 (OR=1.79, p-value=0.0301), and KIR2DL1-HLAC2 (OR=2.10, p-value=0.0175) combinations for complicated malaria.
DUP4 is a complex structural genomic variant that carries extra copies of a glycophorin A-glycophorin B fusion gene and has a dramatic effect on malaria risk by reducing the risk of severe malaria by up to 40%.
One of the positively selected genes, adhesion G protein-coupled receptor E1 (ADGRE1), has also been found to be association with severe malaria resistance in African human populations.
Whereas the receptor-ligand association has revealed risk association against KIR2DS2-HLAC1 (OR=2.08, p-value=0.0229), KIR2DL3-HLAC1 (OR=1.79, p-value=0.0301), and KIR2DL1-HLAC2 (OR=2.10, p-value=0.0175) combinations for complicated malaria.
Our findings provide the new evidence linking circulating BDNF with disease severity, coma recovery and clinical outcome in children with severe malaria.
The means of PKLR, FCGR2A, FCGR2C, and FCGR3 copy numbers were significantly higher among children with severe malaria compared to those with mild malaria (P < .002), indicating that a surplus of copies of those genes is significantly associated with malaria severity.
Haplotype of non-synonymous mutations within IL-23R is associated with susceptibility to severe malaria anemia in a P. falciparum holoendemic transmission area of Kenya.