Trypanosomes and immune evasion
African trypanosomes cause sleeping sickness, a fatal disease of humans and livestock in Africa. During their life cycle, these protozoan parasites cycle between the bloodstream of mammals and tsetse flies. Their two main developmental stages are the bloodstream form and the procyclic form in the tsetse fly. Bloodstream trypanosomes thwart their host’s immune response by periodically switching their major surface protein, the variant surface glycoprotein (VSG). When bloodstream trypanosomes are ingested by a tsetse fly, they must quickly shed the VSG and replace it with an unrelated invariant protein more suited to their survival as procyclic organisms in the fly midgut. This paper examines the mechanisms used by trypanosomes to remove the VSG during their differentiation from bloodstream to procyclic form in culture. Scientists deleted the genes for one of the trypanosome’s protease enzymes from the trypanosome genome and found that bloodstream trypanosomes could still differentiate to the procyclic form, but VSG removal was diminished. Deleting the genes for a phospholipase enzyme had a similar effect – they could still differentiate but VSG removal was impaired. When the genes for both the protease and the phospholipase were deleted, bloodstream trypanosomes could not differentiate to the procyclic form, they retained about 60% of the VSG on their surface, and they died in the differentiation medium. These results highlight the synergistic roles of these two enzymes in the differentiation process.
Tags: Biology, Health, Medicine, Microbiology, Parasitology, Science
Have the terms ‘amastigote’ and ‘promastigote’ forms been replaced?
How many people is sleeping sickness affecting, compared to other African diseases, for example?
Eileen
Dedicated Elementary Teacher Overseas
elementaryteacher.wordpress.com