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A novel functional variant in the stem cell growth factor promoter protects against severe malarial anemia

Collins Ouma1, Christopher C Keller, Gregory C Davenport

  • 1University of New Mexico/KEMRI Laboratories of Parasitic and Viral Diseases, Centre for Global Health Research, Kenya Medical Research Institute, Kisumu, Kenya.

Infection and Immunity
|November 4, 2009
PubMed

Insights

A genetic variant in the stem cell growth factor (SCGF) promoter protects children against severe malarial anemia (SMA). This SCGF promoter variant enhances red blood cell production, reducing the risk of SMA in children with Plasmodium falciparum malaria.

Area of Science:

  • Genetics
  • Hematology
  • Infectious Diseases

Background:

  • Plasmodium falciparum malaria causes significant global health burden, particularly severe malarial anemia (SMA) in children in holoendemic regions like western Kenya.
  • Previous research identified suppressed hematopoietic growth factors, including stem cell growth factor (SCGF), as contributing to SMA development and impaired erythropoiesis.
  • The specific role of SCGF genetic variations in SMA pathogenesis and erythropoietic response remains underexplored.

Purpose of the Study:

  • To investigate the association between a novel SCGF promoter variant (-539C/T, rs7246355) and the incidence of severe malarial anemia (SMA) in Kenyan children.
  • To examine the relationship between this SCGF variant, circulating SCGF levels, and erythropoietic responses, including hemoglobin levels and reticulocyte production index (RPI).
  • To determine if the SCGF promoter variant confers protection against SMA in children infected with Plasmodium falciparum.

Main Methods:

  • A cohort of 486 Kenyan children with falciparum malaria was studied.
  • Genotyping for the SCGF -539C/T promoter variant (rs7246355) was performed.
  • Measurements included circulating SCGF levels, hemoglobin concentration, and reticulocyte production index (RPI). Statistical analyses, including multivariate logistic regression, were employed.

Main Results:

  • Circulating SCGF levels positively correlated with hemoglobin levels and RPI.
  • Children with SMA exhibited significantly lower SCGF levels compared to the non-SMA group.
  • Carriers of the homologous T allele (TT genotype) at the SCGF -539 locus showed protection against SMA (OR=0.57, P=0.027).
  • The TT genotype was associated with higher SCGF levels and an elevated RPI compared to the CC (wild-type) genotype.

Conclusions:

  • The homozygous T allele at the -539 position in the SCGF promoter is linked to increased SCGF production.
  • This genetic variation enhances erythropoiesis and provides a protective effect against the development of severe malarial anemia in children with falciparum malaria.
  • These findings highlight the potential role of specific genetic factors in modulating malaria severity and suggest SCGF as a potential therapeutic target.

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