Abstract
Leishmania infantum causes visceral leishmaniasis, a deadly vector-borne disease introduced to the Americas during the colonial era. This non-native trypanosomatid parasite has since established widespread transmission cycles using alternative vectors, and human infection has become a significant concern to public health, especially in Brazil. A multi-kilobase deletion was recently detected in Brazilian L. infantum genomes and is suggested to reduce susceptibility to the anti-leishmanial drug miltefosine. We show that deletion-carrying strains occur in at least 15 Brazilian states and describe diversity patterns suggesting that these derive from common ancestral mutants rather than from recurrent independent mutation events. We also show that the deleted locus and associated enzymatic activity is restored by hybridization with non-deletion type strains. Genetic exchange appears common in areas of secondary contact but also among closely related parasites. We examine demographic and ecological scenarios underlying this complex L. infantum population structure and discuss implications for disease control.
Highlights
Leishmania infantum causes visceral leishmaniasis, a deadly vector-borne disease introduced to the Americas during the colonial era
Our results reveal the widespread distribution of a major genetic alteration found in New World L. infantum isolates, clarifying that a four-gene deletion on chr[31] predominates in southeastern, eastern, and northeastern Brazil
The extensive evidence of genetic exchange we describe substantiates the importance of this process in trypanosomatid evolution
Summary
Leishmania infantum causes visceral leishmaniasis, a deadly vector-borne disease introduced to the Americas during the colonial era. This non-native trypanosomatid parasite has since established widespread transmission cycles using alternative vectors, and human infection has become a significant concern to public health, especially in Brazil. Rapid changes in genetic makeup can occur and potentially dictate long-term population genetic structure throughout the invasive range[1]. One medically relevant but little explored example of species invasion is represented by the introduction of Leishmania infantum, the parasitic agent of visceral leishmaniasis (VL), into the New World in conjunction with European colonization of the Americas beginning ca.
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