African trypanosomes are flagellated protist parasites transmitted to mammals by the infectious bite of the tsetse fly. They are responsible for sleeping sickness in humans and nagana in cattle. Trypanosomes first proliferate freely in the blood, and then, about six hours after being inoculated, leave the bloodstream to invade various organs, including the skin, which is an anatomic reservoir for the parasites. Few details are known on the metabolic aspects of the different parasite stages in the blood and in the skin, as well as the immune response of the mammalian host against the different stages of development of dermal parasites. Two strains of trypanosomes (“AnTat” and “Lister 427”) with different genetic profiles were studied here: one having only one developmental stage named “SL” or slender in reference to their tapered shape in mice, the second having two developmental stages “SL”, and “ST” for stumpy in reference to their stocky shape in mice. This will allow us to distinguish the transcriptomic signature of parasites at the ST stage. Mice were sampled 5 days or 4 weeks after experimental infection in order to evaluate how the parasite transcriptome evolves over the course of an infection. In all these conditions, blood and skin samples were taken in order to compare the transcriptomes of blood and dermal parasites on the one hand, and transcriptomes of murine blood and dermal tissues on the other. We will especially scrutinize the metabolic pathways of the two parasite strains in the blood and the skin, as well as the immune response of the host in each compartment, two crucial elements determining the development of the infection.
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