Leishmaniasis is an important human and veterinary disease caused by Leishmania parasites that affect 12 million people in over 98 endemic countries. The disease is now emerging in Europe due to climate change and massive population displacement. The parasite is known to rapidly adapt to novel environments with important consequences for disease outcome. It has therefore been recognized as an emerging public health threat for the EU.
In a paper, published in Nature Ecology & Evolution, scientists from the Institut Pasteur in Paris and the Centre for Genomic Regulation (CRG) in Barcelona, in collaboration with teams at the Institute of Tropical Medicine Antwerp (ITM) and the University of Montpellier, have now demonstrated that Leishmania adaptation results from frequent and reversible chromosomal amplifications. Such variations, named aneuploidies, are similar to those occurring in many cancer types.
These findings represent an important step towards a better understanding of human Leishmania infection, with relevance to parasite drug resistance, pathogenicity, and tissue tropism. This novel insight into Leishmania genomic instability should pave the way for the identification of parasite drug resistance mechanisms in clinically relevant settings and help discover biomarkers with diagnostic and prognostic value.
Leishmaniasis is among the five most important parasitic diseases worldwide, with an estimated 350 million people at risk of infection. The disease causes a spectrum of clinical manifestations ranging from disfiguring cutaneous to fatal visceral forms, which results from infection by different species of Leishmania parasites. These unicellular parasites adapt to a remarkable range of hosts. They grow as extracellular parasites inside phlebotomine sand flies that transmit Leishmania to variety of vertebrates, such as rodents, dogs, and humans, where they grow inside immune cells, notably macrophages, causing severe pathologies that may lead to death.