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Mechanisms of Resistance

Reduced Antimony Accumulation in ARM58-Overexpressing Leishmania infantum

Carola Schäfer, Paloma Tejera Nevado, Dorothea Zander, Joachim Clos
Carola Schäfer
Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany
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Paloma Tejera Nevado
Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany
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Dorothea Zander
Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany
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Joachim Clos
Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany
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DOI: 10.1128/AAC.01881-13
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ABSTRACT

Antimony-based drugs are still the mainstay of chemotherapy against Leishmania infections in many countries where the parasites are endemic. The efficacy of antimonials has been compromised by increasing numbers of resistant infections, the basis of which is not fully understood and likely involves multiple factors. By using a functional cloning strategy, we recently identified a novel antimony resistance marker, ARM58, from the parasite Leishmania braziliensis that protects the parasites against antimony-based antileishmanial compounds. Here we show that the Leishmania infantum homologue also confers resistance against antimony but not against other antileishmanial drugs and that its function depends critically on one of four conserved domains of unknown function. This critical domain requires at least two hydrophobic amino acids and is predicted to form a transmembrane structure. Overexpression of ARM58 in antimony-exposed parasites reduces the intracellular Sb accumulation by over 70%, indicating a role for ARM58 in Sb extrusion pathways, but without involvement of energy-dependent transporter proteins.

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Reduced Antimony Accumulation in ARM58-Overexpressing Leishmania infantum
Carola Schäfer, Paloma Tejera Nevado, Dorothea Zander, Joachim Clos
Antimicrobial Agents and Chemotherapy Feb 2014, 58 (3) 1565-1574; DOI: 10.1128/AAC.01881-13

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Reduced Antimony Accumulation in ARM58-Overexpressing Leishmania infantum
Carola Schäfer, Paloma Tejera Nevado, Dorothea Zander, Joachim Clos
Antimicrobial Agents and Chemotherapy Feb 2014, 58 (3) 1565-1574; DOI: 10.1128/AAC.01881-13
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