Human African trypanosomes: challenges posed to the human immune system.

Abstract

Human infection by either Trypanosoma brucei gambiense (Tbg) or Trypanosoma brucei rhodesiense (Tbr) and the establishment of disease is made possible by the intermittent switching of their variant surface glycoprotein (VSG) and expression of serum resistance associated (SRA) protein (by Tbr) which nullifies the lytic action of the normal human serum. The ability to switch expression from one VSG to the other is recognized to be the major mechanism that permits the parasite to evade the otherwise efficient host antibody, hence preventing parasite elimination and allowing the establishment of a chronic infection. These changes were reported to: disable the host's capacity to mount a protective anti-parasite antibody response and prevent the development of effective B-cell memory against encountered variant antigenic parasite types (VATs). Both B cell-mediated antibody response and the Th1 cell responses leading to the production of interferon-gamma (IFN-) are required for maximum host resistance to trypanosomes, with IFN-acting to induce macrophage trypanolytic and trypanostatic activities. High levels of both tumor necrosis factor alpha (TNF) and interleukin 10 (IL-10) have been associated with trypanosomal infection. Trypanosomal genetics (including the parasite's intrinsic characteristics), human immune response polymorphisms and geographical locations are important elements that describe the severity or mildness of HAT. As the parasite devices ways to evade the human immune system, and in the absence of a suitable vaccine, surveillance, prompt diagnosis and treatment with available drugs and vector control efforts will go along way in reducing the incidence of HAT.

Epidemiology of tsetse flies in the transmission of trypanosomiasis: technical review of The Gambia experience

“…About 50 million cattle and 70 million sheep and goats are at risk for AAT and an estimated three million cattle die from the disease annually in Africa (Simarro et al, 2010). As the parasite maneuvers ways to avoid the animal's immune system, and in the absence of a suitable vaccine, surveillance, speedy diagnosis and treatment with existing drugs are not effective and vector control efforts will go a long way in decreasing the incidence of AAT (Oyibo et al, 2009;Zongo et al, 2016). AAT still remains by far the most devastating parasitic and neglected zoonotic disease in Africa, affecting both humans and livestock.…”

RNA interference: recent trends and its application in controlling Neglected Tropical Diseases (NTDs)

“…The trypanosomes life cycle is an intermediate between the tsetse fly and its mammalian host (Ebene et al, 2016;Mamoudou et al, 2016) RNAi was used to examine the role of a specific gene in tsetse flies (Nayduch and Aksoy, 2007). Tsetse flies, Glossina spp., transmit African trypanosomes which includes Africa Animal Trypanosomiasis and Human African Trypanosomiasis but the prevalence is low because the flies are refractory to trypanosome infection (Oyibo et al, 2009). Scientists have compared the transcription levels of an antimicrobial peptide gene attacin, between refractory G. palpalis palpalis and susceptible G. morsitans morsitans.…”

Influence of environmental conditions on mass rearing parameters of tsetse flies at the Bobo-Dioulasso insectary (Burkina Faso): Retrospective study

“…AAT constitute one of the major constraints to the socio-economic development of sub-Saharan Africa because meat production is reduced by 30%, milk production by 40% and labour power can be reduced by a third (FAO, 2002). HAT is challenging to the human immune system (Oyibo et al, 2009). For the more, the cost of treatment is not insignificant because at least 25-30 million doses of trypanocides are used each year (Vreysen, 2006).…”