Unexpected plasticity in the life cycle of Trypanosoma brucei

• DOI: 10.7554/elife.66028
• Publication Date: 2021-08-06T12:00:23Z
• Authors: Sarah Schuster; Jaime Lisack; Ines Subota; Henriette Zimmermann; Christian Reuter; Tobias Mueller; Brooke Morriswood; Markus Engstler
• Keywords: Male; Microbiology and Infectious Disease; Life Cycle Stages; Tsetse Flies; QH301-705.5; sleeping sickness; Science; Q; Trypanosoma brucei brucei; transmission; R; Protozoan Proteins; Host-Parasite Interactions; Gastrointestinal Tract; life cycle; Medicine; Animals; Female; ddc:570; tsetse fly; RNA, Messenger; Biology (General); development; RNA, Protozoan; trypanosoma

African trypanosomes cause sleeping sickness in humans and nagana cattle. These unicellular parasites are transmitted by the bloodsucking tsetse fly. In mammalian host's circulation, proliferating slender stage cells differentiate into cell cycle-arrested stumpy when they reach high population densities. This transition is thought to fulfil two main functions: first, it auto-regulates parasite load host; second, regarded as only capable of successful vector transmission. Here, we show that express mRNA protein a known marker, complete complex life cycle fly successfully stage, require single for productive infection. findings suggest reassessment traditional view trypanosome cycle. They may also provide solution long-lasting paradox, namely transmission chronic infections, despite low parasitemia.