Authors

L Figueiredo²; S Trindade²; M De Niz³; H Machado²; L Lopez-Escobar²; R Zechner⁴; T Smith¹; C Franco⁵;  ¹ University of St Andrews, UK;  ² Instituto de medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Portugal;  ³ Center for Advanced Microscopy and Nikon Imaging Center, Northwestern University, United States;  ⁴ Institute of Molecular Biosciences, University of Graz, Austria;  ⁵ Catolica Biomedical Research Centre, Lisboa, Portugal

Discussion

Trypanosoma brucei crosses blood vessels and colonises multiple tissues. Adipose tissue is one of the largest reservoirs in mouse models. In this talk, I will discuss the molecular basis for this preferential colonisation, the consequences for the host, and potential benefits for the parasite. Using tools like intravital microscopy and mouse genetic models, we have identified key host surface receptors required for colonisation and shown that adipocyte lipolysis activation is in part responsible for loss of fat mass during infection. Proteomics and novel methods to quantify parasite proliferation in vivo have revealed that parasites adapt to the tissue microenvironment and may enter a persistence stage. These insights enhance our understanding of the evolutionary dynamics of host-parasite interactions and the mechanisms underlying disease relapse