1. Genetics and Genomics
  2. Microbiology and Infectious Disease
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Gene Variation: The double-edged sword of evolution

  1. Etty Kruzel-Davila
  2. Karl Skorecki  Is a corresponding author
  1. Rambam Health Care Campus, Israel
  2. Rambam Heath Care Campus, Israel
  3. Technion – Israel Institute of Technology, Israel
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Cite this article as: eLife 2017;6:e29056 doi: 10.7554/eLife.29056
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Figures

Individuals carrying different variants of the APOL1 gene are protected against sleeping sickness and kidney disease to different extents.

Individuals with two copies of wild-type APOL1 (G0 homozygotes) are not protected against sleeping sickness caused by T. b. rhodesiense (red figure, left column) or T. b. gambiense (red figure, middle column), but they do not have an increased risk of chronic kidney disease - CKD (yellow figure, right column). Individuals with one copy of wild-type APOL1 and one copy of the G1 variant (G1 heterozygotes), and individuals with two copies of the G1 variant (G1 homozygotes) are not protected against sleeping sickness caused by T. b. rhodesiense (second red figure, left column) and are more likely to have latent asymptomatic infection by T. b. gambiense (pink figure, middle column). Individuals with one copy of wild-type APOL1 and one copy of the G2 variant (G2 heterozygotes), and individuals with two copies of the G2 variant (G2 homozygotes) are protected against sleeping sickness caused by T. b. rhodesiense (green figure, left column) but are at increased risk of developing symptomatic infection by T. b. gambiense (grey figure, middle column). Like G0 homozygotes, G1 heterozygotes and G2 heterozygotes do not have an increased risk of chronic kidney disease (second yellow figure, right column). However, G1 homozygotes, G2 homozygotes and compound heterozygotes (individuals with both G1 and G2) all have an increased risk of chronic kidney disease (blue figure, right column).

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