Unexpected plasticity in the life cycle of Trypanosoma brucei

Elife. 2021 Aug 6:10:e66028. doi: 10.7554/eLife.66028.

Abstract

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

Keywords: development; infectious disease; life cycle; microbiology; sleeping sickness; transmission; trypanosoma; tsetse fly.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Female
  • Gastrointestinal Tract / parasitology
  • Host-Parasite Interactions / physiology
  • Life Cycle Stages / physiology*
  • Male
  • Protozoan Proteins / metabolism
  • RNA, Messenger / metabolism
  • RNA, Protozoan / metabolism
  • Trypanosoma brucei brucei* / pathogenicity
  • Trypanosoma brucei brucei* / physiology
  • Tsetse Flies / parasitology

Substances

  • Protozoan Proteins
  • RNA, Messenger
  • RNA, Protozoan

Grants and funding

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.