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Related Experiment Video

Updated: Jul 3, 2026

Purification of Extracellular Trypanosomes, Including African, from Blood by Anion-Exchangers (Diethylaminoethyl-cellulose Columns)

Purification of Extracellular Trypanosomes, Including African, from Blood by Anion-Exchangers (Diethylaminoethyl-cellulose Columns)

Published on: April 6, 2019

Mutual self-defence: the trypanolytic factor story.

Etienne Pays¹, Benoit Vanhollebeke

¹Laboratory of Molecular Parasitology, Université Libre de Bruxelles, Gosselies, Belgium. epays@ulb.ac.be

Microbes and Infection

|August 5, 2008

Summary

Human serum contains apolipoprotein L1 (apoL1) that lyses Trypanosoma brucei brucei. Some parasites resist this by internalizing Serum Resistance-Associated (SRA) protein, which neutralizes apoL1, causing sleeping sickness.

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Area of Science:

Parasitology
Immunology
Biochemistry

Background:

African trypanosomes, like Trypanosoma brucei brucei, are lysed by a factor in human and ape blood.
This trypanolytic factor is a complex involving apolipoprotein L1 (apoL1) and haptoglobin-related protein (Hpr) on HDL particles.
Parasite uptake of Hpr-containing HDL leads to apoL1 internalization and lysosomal pore formation, causing parasite death.

Purpose of the Study:

To elucidate the mechanism of human serum-mediated lysis of Trypanosoma brucei.
To understand how certain Trypanosoma brucei clones resist this lysis and cause human sleeping sickness.
To explore therapeutic strategies against human-infecting trypanosomes based on host-parasite interactions.

Main Methods:

Biochemical analysis of serum factors and parasite surface receptors.
Cellular localization studies of apoL1 and parasite proteins.
Genetic and protein interaction studies to identify resistance mechanisms.

Main Results:

Human and ape serum contains apoL1, a trypanolytic factor that forms pores in parasite lysosomes.
Trypanosoma brucei brucei is lysed by apoL1, while Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense are resistant.
Serum Resistance-Associated (SRA) protein in T. b. rhodesiense neutralizes apoL1 in endosomes, conferring resistance.

Conclusions:

ApoL1-mediated lysis is a key defense mechanism against T. b. brucei in humans.
The SRA protein of T. b. rhodesiense represents a novel mechanism of parasite resistance to host immunity.
Understanding these interactions offers potential targets for treating human African trypanosomiasis.