This led to the realization that many of the existing therapies now available to fight African sleeping sickness are often ineffective and have extreme toxicity, frequently causing death. Additionally, there is increasing evidence that while new therapeutics may cure the disease, long-lasting neurological damage can be caused by infection.
The World Health Organization reports that the recent introduction of aggressive population screening in rural areas and distribution of more effective drugs has dramatically reduced the number of deaths, however.
Several species of African trypanosomes infect non-primate mammals and cause important veterinary disease yet are unable to infect humans. The trypanosomes that cause human disease, Trypanosoma brucei gambiense and T. b. rhodensiense, have evolved mechanisms to avoid the native human defense molecules in the circulatory system that kill the parasites that cause animal disease.
Two of the major challenges faced by scientists studying human sleeping sickness have been the identification of the naturally occurring human defense molecules that are active against the trypanosomes causing animal disease, and the identification of the strategies used by the human sleeping sickness parasites to avoid the action of these molecules.
Human innate immunity against most African trypanosomes is mediated by a subclass of HDL (high density lipoprotein, which people know from blood tests as "good cholesterol") called trypanosome lytic f
|Contact: Stephen Hajduk|
University of Georgia