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Updated: May 17, 2026
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Purification of Extracellular Trypanosomes, Including African, from Blood by Anion-Exchangers (Diethylaminoethyl-cellulose Columns)
Published on: April 6, 2019
[Molecular dialogue between African trypanosomes and humans]
1Laboratoire de Parasitologie moléculaire, IBMM, ULB.
Bulletin Et Memoires De L'Academie Royale De Medecine De Belgique
|October 23, 2012
Summary
Human serum contains apolipoprotein L1 (apoL1), which kills African trypanosomes. Natural apoL1 mutations offer protection against sleeping sickness but can cause kidney disease.
Area of Science:
- Human evolutionary biology
- Parasitology
- Immunology
Background:
- Human serum possesses innate immunity against African trypanosomes, the cause of sleeping sickness.
- Two pathogenic clones, T. b. rhodesiense and T. b. gambiense, evade this immunity.
- Apolipoprotein L1 (apoL1) bound to HDL particles is identified as the trypanolytic factor.
Discussion:
- ApoL1, along with haptoglobin-related protein (Hpr), is taken up by trypanosomes via the Hp-Hb complex receptor.
- Inside the parasite, apoL1 forms pores in the lysosomal membrane, leading to cell death.
- Engineered apoL1 mutants resist parasite neutralization and kill T. b. rhodesiense.
Key Insights:
- Naturally occurring apoL1 mutants exist in populations of African origin.
- A single apoL1 mutant allele provides protection against T. b. rhodesiense infection.
- Dual alleles of these mutants increase the risk of end-stage renal disease.
Outlook:
- The study highlights natural selection favoring trypanosome resistance despite kidney risks.
- Mechanisms linking mutant apoL1 to kidney disease are under investigation.
- Understanding apoL1's role is crucial for human evolution and disease research.
