Dance Of The Sugar Plum Fairy-Antigenic Variation In African Trypanosomes

Introduction

The immune system of humans and other higher organisms has developed into an intricate network of responses to a panoply of invading organisms that challenge their hosts (Schmid-Hempel, 2008). This arms race originating from a dynamic and never-ending battle between hosts and pathogens (i.e. between proverbial “good guys” and “bad guys”), where countermeasures and innovative strategies are being endlessly generated throughout evolutionary history, is considered the prime reason why our immune systems are so complex (Schmid-Hempel, 2009). Although anthropomorphization should be avoided, we are not mistaken if we say the parasite’s intent is to survive in adverse environment long enough to ensure progeny for the continuation of
Host immune responses and parasitic immune evasion stratagems employed by various pathogens infecting humans. Reproduced from: Schmid-Hempel, P. (2008). Parasite immune evasion: a momentous molecular war. Trends in Ecology & Evolution 2008; 23: 318-26.
Dance of the Sugar Plum Fairy – Antigenic Variation in African Trypanosomes

Trypanosoma brucei (T. brucei) is a protozoan parasite transmitted by the biting tsetse flies from to the genus Glossina, primarily known for infecting mammals in sub-Saharan African region (Mugnier et al., 2016). Two subspecies of the parasite – namely T. brucei gambiense and T. brucei rhodesiense – cause a potentially fatal disease in humans known as African trypanosomiasis. The other notable subspecies, T. brucei brucei, infects animals with a substantial economic burden to this already impoverished part of the world (Mugnier et al., 2016). This parasitic species lives outside cells in blood and tissues of infected mammalian hosts, and is able to survive in such harsh environment due to variant surface glycoprotein (VSG) – an abundant and dense proteinaceous layer that overlays the plasma membrane (Horn, 2014). Glycoproteins are basically proteins with covalently attached sugar residues, and repeated replacement of VSG in Trypanosoma brucei (figuratively analogous to frequent coat changing) gives a significant edge in the evolutionary cat-and-mouse game (McCulloch & Field,
During the infectious process there is a continuous antigenic variation where the parasite “switches” VSG expression by dipping into a genomic repertoire containing more than one thousand VSG-encoding genes, which aids in being one step ahead of the host’s immune system (Pinger et al., 2017). The produced antibodies may indeed successfully neutralize and destroy approximately 99 percent of the Trypanosoma population; nevertheless, during this attack few parasites may shed their coat (in other words, switch VSG) and cover themselves with a novel, antigenically distinct VSG (Horn, 2014). Subsequently they become a source of a new clonal population of parasites which proliferate and repeat this whole process, as a small portion of Trypanosoma can always render themselves undetectable in order to evade mounted immune