Author:
CAPEWELL PAUL,COOPER ANNELI,CLUCAS CAROLINE,WEIR WILLIAM,MACLEOD ANNETTE
Abstract
SUMMARYTrypanosoma brucei is the causative agent of African sleeping
sickness in humans and one of several pathogens that cause the related
veterinary disease Nagana. A complex co-evolution has occurred between these
parasites and primates that led to the emergence of trypanosome-specific
defences and counter-measures. The first line of defence in humans and several
other catarrhine primates is the trypanolytic protein
apolipoprotein-L1 (APOL1) found within two serum protein complexes, trypanosome
lytic factor 1 and 2 (TLF-1 and TLF-2). Two sub-species of T.
brucei have evolved specific mechanisms to overcome this innate
resistance, Trypanosoma brucei gambiense and
Trypanosoma brucei rhodesiense. In T. b.
rhodesiense, the presence of the serum resistance associated
(SRA) gene, a truncated variable surface glycoprotein
(VSG), is sufficient to confer resistance to lysis. The resistance mechanism of
T. b. gambiense is more complex, involving multiple
components: reduction in binding affinity of a receptor for TLF, increased
cysteine protease activity and the presence of the truncated VSG, T. b.
gambiense-specific glycoprotein (TgsGP). In a
striking example of co-evolution, evidence is emerging that primates are
responding to challenge by T. b. gambiense and T. b.
rhodesiense, with several populations of humans and primates
displaying resistance to infection by these two sub-species.
Publisher
Cambridge University Press (CUP)
Subject
Infectious Diseases,Animal Science and Zoology,Parasitology
Cited by
47 articles.
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